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mouse cxcl12 sdf 1 alpha quantikine elisa kit (R&D Systems)

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R&D Systems mouse cxcl12 sdf 1 alpha quantikine elisa kit
Mouse Cxcl12 Sdf 1 Alpha Quantikine Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 139 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+cxcl12/Mouse+CXCL12%2FSDF-1+alpha+Quantikine+ELISA+Kit/bio_rxiv__64898__2026__04__21__720007-284-6-12
Average 95 stars, based on 139 article reviews

mouse cxcl12 sdf 1 alpha quantikine elisa kit - by Bioz Stars, 2026-09

95/100 stars

Images

Blocking Assay:

Article Title: CXCR4 induces memory formation over exhaustion in CAR-T cells to achieve durable leukemia targeting.
Article Snippet: Non-specific background was reduced by incubating the slides in methanol and H2O2 (Wako). .. After blocking with horse serum, slides were incubated with mouse antihumanTCF1 antibody (R&D systems, #2203) (1:200), anti-humanCD33 (R&D systems, MAB11371) (1:100), anti-human and mouse CXCL12 (R&D systems, MAB350) (1:20), or anti-human CCR7 (Abcam, ab253187) (1:100) and then HRP-conjugated horse anti-rabbit or antimouse IgG antibody (ImmPRESS, MP-7500). .. Slides were then stained with 3,3′-diaminobenzine or hematoxylin and eosin, dehydrated, mounted using VectaMount (Vector Laboratories) and analyzed with the Axiovert 200 microscope (Zeiss).

Article Title: CXCR4 induces memory formation over exhaustion in CAR-T cells to achieve durable leukemia targeting
Article Snippet: Non-specific background was reduced by incubating the slides in methanol and H 2 O 2 (Wako). .. After blocking with horse serum, slides were incubated with mouse anti-human TCF1 antibody (R&D systems, #2203) (1:200), anti-human CD33 (R&D systems, MAB11371) (1:100), anti-human and mouse CXCL12 (R&D systems, MAB350) (1:20), or anti-human CCR7 (Abcam, ab253187) (1:100) and then HRP-conjugated horse anti-rabbit or anti-mouse IgG antibody (ImmPRESS, MP-7500). .. Slides were then stained with 3,3′-diaminobenzine or hematoxylin and eosin, dehydrated, mounted using VectaMount (Vector Laboratories) and analyzed with the Axiovert 200 microscope (Zeiss).

Incubation:

Enzyme-linked Immunosorbent Assay:

Article Title: A Selective Neutraligand for CXCL12/SDF-1α With Beneficial Regulatory Functions in MRL/Lpr Lupus Prone Mice.
Article Snippet: .. The ELISA kit for mouse CXCL12 (R&D Systems, ref. DY460; kit range: 46–3,000 pg/mL; sensitivity: 23 pg/mL) was used according to the manufacturer’s instructions. ..

Article Title: A Selective Neutraligand for CXCL12/SDF-1α With Beneficial Regulatory Functions in MRL/Lpr Lupus Prone Mice
Article Snippet: .. The ELISA kit for mouse CXCL12 (R&D Systems, ref. DY460; kit range: 46–3,000 pg/mL; sensitivity: 23 pg/mL) was used according to the manufacturer’s instructions. ..

Article Title: Endothelial protein C receptor CD201 is a better marker than SCA1 to identify mouse long-term reconstituting hematopoietic stem cells following septic challenge.
Article Snippet: Stem cell antigen-1 (SCA1) is widely used to identify mouse hematopoietic stem cells (HSC) and multipotent progenitors (MPP) among lineage-negative KIT (LK) cells.. However, SCA1 is expressed only in a few inbred mouse strains and becomes strongly upregulated on LK cells following in vivo challenge with interferons, lipopolysaccharide (LPS) or pathogens leading to incorrect analysis of HSC function subsets and delineation of HSC, MPP and lineage-restricted progenitor subsets.. Endothelial protein C receptor CD201can be used as an alternative marker for mouse and even human HSC.

Article Title: Endothelial protein C receptor CD201 is a better marker than SCA1 to identify mouse long-term reconstituting hematopoietic stem cells following septic challenge
Article Snippet: .. Mouse CXCL12 was quantified using specific ELISA kits (R&D Systems; cat # MCX120) in BM fluids following manufacturer’s instructions. .. Plates were read with plate reader (Thermo Fisher Scientific) according to manufacturer’s instructions.

Recombinant:

Article Title: Critical role of WNK1 in MYC-dependent early mouse thymocyte development
Article Snippet: Peptide, recombinant protein , Streptavidin-PerCP , Biolegend , Cat #: 405213 , FACS (1:200). .. Peptide, recombinant protein , mouse CXCL12 , R and D systems , Cat # 460-SD-010/CF , (500 ng/ml). .. Peptide, recombinant protein , mouse ICAM1-Fc , R and D systems , Cat # 796-IC-050 , Transwell assay (500 ng/ml); Adhesion Assay (25 μg/ml).

Migration:

Article Title: PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration
Article Snippet: In brief, the inverted 5 μm pore size transwell insert (24-well, Corning International) was coated with 0.2% (w/v) gelatin (Bio-Rad) before loading with 1 × 10 5 LECs. .. Before migration, 2 × 10 5 migrating cells in 100 μL were loaded into the upper chamber of the transwell plate while the lower chamber contained 50 ng/mL mCCL19 (R&D systems), 100 ng/mL hCCL19 (R&D systems), 500 ng/mL mouse CXCL12 (R&D systems), 500 ng/mL mouse CCL21 (R&D systems), or 200 nM S1P (Sigma–Aldrich). ..

Image Search Results

Serum CXCL12 is significantly elevated in PNI patients at 72 hours post-operation. The expression level of CXCL12 in the serum was analyzed via ELISA. The data are presented as the means ± SDs, n=20, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: Serum CXCL12 is significantly elevated in PNI patients at 72 hours post-operation. The expression level of CXCL12 in the serum was analyzed via ELISA. The data are presented as the means ± SDs, n=20, **** p < 0.0001

Article Snippet: Investigation of the effect of CXCL12 (Sino Biological, 50025-MNAE, China) on SCs ferroptosis and inflammatory response: SCs were divided into Control group, LPS group, and LPS + CXCL12 group.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

CXCL12 inhibits LPS-induced ferroptosis in SCs. ( A ) Effect of different concentrations of LPS on SC survival levels. ( B ) Effect of different concentrations of CXCL12 on SC survival levels after LPS-induced SC damage. ( C - E ) RT-qPCR analysis of mRNA expression levels of ferroptosis-related genes (ACSL4, GPX4, FSP1) in SCs after CXCL12 treatment. (F) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after CXCL12 treatment. ( G - I ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. ( J , K ) Immunofluorescence analysis of the expression levels of ferroptosis-related proteins ACSL4 and GPX4 in SCs after CXCL12 treatment, Scale bar = 100 um. ( L , M ) Quantification of the relative fluorescence intensity of ACSL4 and GPX4. ( N , O ) Fluorescence images of ROS and Fe 2+ in SCs after CXCL12 treatment, Scale bar = 50 um. ( P , Q ) Quantification of the relative fluorescence intensity of ROS and Fe 2+ . ( R , S ) Expression levels of MDA and GSH in SCs after CXCL12 treatment. The data are presented as the means±SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits LPS-induced ferroptosis in SCs. ( A ) Effect of different concentrations of LPS on SC survival levels. ( B ) Effect of different concentrations of CXCL12 on SC survival levels after LPS-induced SC damage. ( C - E ) RT-qPCR analysis of mRNA expression levels of ferroptosis-related genes (ACSL4, GPX4, FSP1) in SCs after CXCL12 treatment. (F) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after CXCL12 treatment. ( G - I ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. ( J , K ) Immunofluorescence analysis of the expression levels of ferroptosis-related proteins ACSL4 and GPX4 in SCs after CXCL12 treatment, Scale bar = 100 um. ( L , M ) Quantification of the relative fluorescence intensity of ACSL4 and GPX4. ( N , O ) Fluorescence images of ROS and Fe 2+ in SCs after CXCL12 treatment, Scale bar = 50 um. ( P , Q ) Quantification of the relative fluorescence intensity of ROS and Fe 2+ . ( R , S ) Expression levels of MDA and GSH in SCs after CXCL12 treatment. The data are presented as the means±SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Immunofluorescence, Fluorescence

CXCL12 activates the ERK/Nrf2 signaling pathway in SCs. ( A ) Western blot analysis of ERK, p-ERK, and Nrf2 protein expression levels in SCs after CXCL12 treatment. ( B - C ) Quantification of the gray values for the ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 proteins. The data are presented as the means ± SDs, n=3, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 activates the ERK/Nrf2 signaling pathway in SCs. ( A ) Western blot analysis of ERK, p-ERK, and Nrf2 protein expression levels in SCs after CXCL12 treatment. ( B - C ) Quantification of the gray values for the ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 proteins. The data are presented as the means ± SDs, n=3, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Techniques: Western Blot, Expressing

CXCL12 inhibits SC ferroptosis via the ERK/Nrf2 signaling pathway. ( A ) Western blot analysis of Nrf2 expression levels in SCs after treatment with the ERK inhibitor U0126. ( B ) Densitometric analysis of Nrf2 protein. ( C ) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after treatment with the ERK inhibitor U0126. ( D - F ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits SC ferroptosis via the ERK/Nrf2 signaling pathway. ( A ) Western blot analysis of Nrf2 expression levels in SCs after treatment with the ERK inhibitor U0126. ( B ) Densitometric analysis of Nrf2 protein. ( C ) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after treatment with the ERK inhibitor U0126. ( D - F ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Techniques: Western Blot, Expressing

CXCL12 inhibits NF-κB signaling pathway activation and inflammatory factor secretion in SCs. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in SCs after CXCL12 treatment. ( B - C ) Quantification of gray values for the NF-κB, p-NF-κB, κBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in SCs after CXCL12 treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits NF-κB signaling pathway activation and inflammatory factor secretion in SCs. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in SCs after CXCL12 treatment. ( B - C ) Quantification of gray values for the NF-κB, p-NF-κB, κBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in SCs after CXCL12 treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Techniques: Activation Assay, Western Blot, Expressing

CXCL12 inhibits the inflammatory response in SCs via the NF-κB signaling pathway. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in SCs after NF-κB overexpression. ( B - C ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in SCs after NF-κB overexpression. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits the inflammatory response in SCs via the NF-κB signaling pathway. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in SCs after NF-κB overexpression. ( B - C ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in SCs after NF-κB overexpression. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Techniques: Western Blot, Expressing, Over Expression

CXCL12 inhibits SC ferroptosis, thereby mitigating the inflammatory response. ( A ) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after FAC treatment. ( B - D ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. ( E , F ) Fluorescence images of ROS and Fe 2+ in SCs after FAC treatment, Scale bar = 50µm. ( G , H ) Quantification of the relative fluorescence intensity of ROS and Fe 2+ . ( I , J ) Expression levels of MDA and GSH in SCs after FAC treatment. ( K ) Western blot analysis of the expression levels of NF-κB, p-NF-κB, IκBα, and p-IκBα in SCs after FAC treatment. ( L , M ) Densitometric analysis of proteins NF-κB, p-NF-κB, IκBα, and p-IκBα. ( N , O ) Expression levels of IL-1β and TNF-α in SCs after FAC treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits SC ferroptosis, thereby mitigating the inflammatory response. ( A ) Western blot analysis of the expression levels of ferroptosis-related proteins ACSL4, GPX4, and FSP1 in SCs after FAC treatment. ( B - D ) Densitometric analysis of proteins ACSL4, GPX4, and FSP1. ( E , F ) Fluorescence images of ROS and Fe 2+ in SCs after FAC treatment, Scale bar = 50µm. ( G , H ) Quantification of the relative fluorescence intensity of ROS and Fe 2+ . ( I , J ) Expression levels of MDA and GSH in SCs after FAC treatment. ( K ) Western blot analysis of the expression levels of NF-κB, p-NF-κB, IκBα, and p-IκBα in SCs after FAC treatment. ( L , M ) Densitometric analysis of proteins NF-κB, p-NF-κB, IκBα, and p-IκBα. ( N , O ) Expression levels of IL-1β and TNF-α in SCs after FAC treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant

Techniques: Western Blot, Expressing, Fluorescence

CXCL12 inhibits PNI-induced ferroptosis in SCs. (A) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after CXCL12 treatment. (B-D) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. (E-F) Representative immunofluorescence images of the ferroptosis-related proteins ACSL4 and GPX4 in the sciatic nerve after CXCL12 treatment. Scale bar = 50 µm. (G, H) Quantification of the relative fluorescence intensities of ACSL4 and GPX4. (I-K) Levels of Fe2+, MDA, and GSH in the sciatic nerve after CXCL12 treatment. (L-M) Transmission electron microscopy images showing the condition of the mitochondria in the SCs of the sciatic nerve after CXCL12 treatment. The data are presented as the means ± SDs, n=3, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits PNI-induced ferroptosis in SCs. (A) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after CXCL12 treatment. (B-D) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. (E-F) Representative immunofluorescence images of the ferroptosis-related proteins ACSL4 and GPX4 in the sciatic nerve after CXCL12 treatment. Scale bar = 50 µm. (G, H) Quantification of the relative fluorescence intensities of ACSL4 and GPX4. (I-K) Levels of Fe2+, MDA, and GSH in the sciatic nerve after CXCL12 treatment. (L-M) Transmission electron microscopy images showing the condition of the mitochondria in the SCs of the sciatic nerve after CXCL12 treatment. The data are presented as the means ± SDs, n=3, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Techniques: Western Blot, Expressing, Immunofluorescence, Fluorescence, Transmission Assay, Electron Microscopy

CXCL12 activates the ERK/Nrf2 signaling pathway in the sciatic nerve. ( A ) Western blot analysis of ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 protein expression levels in the sciatic nerve after CXCL12 treatment. ( B - C ) Quantification of the gray values for the ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 proteins. The data are presented as the means ± SDs, n=3, ** p < 0.01,*** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 activates the ERK/Nrf2 signaling pathway in the sciatic nerve. ( A ) Western blot analysis of ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 protein expression levels in the sciatic nerve after CXCL12 treatment. ( B - C ) Quantification of the gray values for the ERK, p-ERK, Total Nrf2 and Nuclear Nrf2 proteins. The data are presented as the means ± SDs, n=3, ** p < 0.01,*** p < 0.001, **** p < 0.0001

Techniques: Western Blot, Expressing

CXCL12 inhibits ferroptosis in the sciatic nerve via the ERK/Nrf2 signaling pathway. ( A ) Western blot analysis of Nrf2 protein expression levels in the sciatic nerve after treatment with the ERK inhibitor U0126. ( B ) Quantification of the gray values for the Nrf2 protein. ( C ) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after treatment with the ERK inhibitor U0126. ( D - F ) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits ferroptosis in the sciatic nerve via the ERK/Nrf2 signaling pathway. ( A ) Western blot analysis of Nrf2 protein expression levels in the sciatic nerve after treatment with the ERK inhibitor U0126. ( B ) Quantification of the gray values for the Nrf2 protein. ( C ) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after treatment with the ERK inhibitor U0126. ( D - F ) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Techniques: Western Blot, Expressing

CXCL12 inhibits NF-κB signaling pathway activation and inflammatory factor secretion in the sciatic nerve. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in the sciatic nerve after CXCL12 treatment. ( B - C ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in the sciatic nerve after CXCL12 treatment. The data are presented as the means ± SDs, n=3, **p < 0.01, ***p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits NF-κB signaling pathway activation and inflammatory factor secretion in the sciatic nerve. ( A ) Western blot analysis of NF-κB, p-NF-κB, IκBα, and p-IκBα protein expression levels in the sciatic nerve after CXCL12 treatment. ( B - C ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα, and p-IκBα proteins. ( D - E ) Levels of IL-1β and TNF-α in the sciatic nerve after CXCL12 treatment. The data are presented as the means ± SDs, n=3, **p < 0.01, ***p < 0.001, **** p < 0.0001

Techniques: Activation Assay, Western Blot, Expressing

CXCL12 inhibits sciatic nerve ferroptosis, thereby mitigating the inflammatory response. ( A ) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after FAC treatment. ( B - D ) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. ( E ‒ G ) Levels of Fe 2+ , MDA, and GSH in the sciatic nerve after FAC treatment. ( H ) Western blot analysis of NF-κB, p-NF-κB, IκBα and p-IκBα protein expression levels in the sciatic nerve after FAC treatment. ( I , J ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα and p-IκBα proteins. (K, L) Levels of IL-1β and TNF-α in the sciatic nerve after FAC treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 inhibits sciatic nerve ferroptosis, thereby mitigating the inflammatory response. ( A ) Western blot analysis of ferroptosis-related protein expression levels (ACSL4, GPX4, FSP1) in the sciatic nerve after FAC treatment. ( B - D ) Quantification of the gray values for the ACSL4, GPX4, and FSP1 proteins. ( E ‒ G ) Levels of Fe 2+ , MDA, and GSH in the sciatic nerve after FAC treatment. ( H ) Western blot analysis of NF-κB, p-NF-κB, IκBα and p-IκBα protein expression levels in the sciatic nerve after FAC treatment. ( I , J ) Quantification of the gray values for the NF-κB, p-NF-κB, IκBα and p-IκBα proteins. (K, L) Levels of IL-1β and TNF-α in the sciatic nerve after FAC treatment. The data are presented as the means ± SDs, n=3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Techniques: Western Blot, Expressing

CXCL12 promotes nerve regeneration after PNI. ( A ) PWT. ( B ) PWL. ( C ) Representative footprint images of rats post-surgery. ( D ) SFI. ( E ) H&E staining of the longitudinal section of the sciatic nerve. ( F ) Immunofluorescence images of MBP and NF200 in the sciatic nerve. ( G , H ) Quantification of the relative fluorescence intensity of proteins MBP and NF200. The data are presented as the means ± SDs, n=3, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Inflammation

Article Title: CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway

doi: 10.1007/s10753-026-02453-2

Figure Lengend Snippet: CXCL12 promotes nerve regeneration after PNI. ( A ) PWT. ( B ) PWL. ( C ) Representative footprint images of rats post-surgery. ( D ) SFI. ( E ) H&E staining of the longitudinal section of the sciatic nerve. ( F ) Immunofluorescence images of MBP and NF200 in the sciatic nerve. ( G , H ) Quantification of the relative fluorescence intensity of proteins MBP and NF200. The data are presented as the means ± SDs, n=3, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Techniques: Staining, Immunofluorescence, Fluorescence

Substrate stiffness regulates the behaviors of human gingival fibroblasts (HGFs). Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect gene expression levels of (A) anti-inflammatory markers, IL4 , and IL10 , (B) matrix metalloproteinase markers, including MMP9 , and TIMP1 , (C) chemokine, CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The protein expression of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL4, interleukin 4; IL10, interleukin 10; MMP9, matrix metalloproteinase 9; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells

doi: 10.3389/fbioe.2026.1753774

Figure Lengend Snippet: Substrate stiffness regulates the behaviors of human gingival fibroblasts (HGFs). Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect gene expression levels of (A) anti-inflammatory markers, IL4 , and IL10 , (B) matrix metalloproteinase markers, including MMP9 , and TIMP1 , (C) chemokine, CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The protein expression of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL4, interleukin 4; IL10, interleukin 10; MMP9, matrix metalloproteinase 9; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Article Snippet: CXCL12 protein in conditioned medium was measured by Human CXCL12/SDF-1α ELISA Kit (Quantikine, R&D systems.

Techniques: Reverse Transcription, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Expressing, Control, Comparison, Enzyme-linked Immunosorbent Assay, Standard Deviation

Substrate stiffness regulates human gingival fibroblasts (HGFs) behaviors under an inflammatory condition. Real-time RT-PCR was performed to detect gene expression levels of (A) IL4 and IL10 , (B) MMP9 and TIMP1 , and (C) CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The expression protein of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL4, interleukin 4; IL10, interleukin 10; MMP9, matrix metalloproteinase 9; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane; LPS, lipopolysaccharide.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells

doi: 10.3389/fbioe.2026.1753774

Figure Lengend Snippet: Substrate stiffness regulates human gingival fibroblasts (HGFs) behaviors under an inflammatory condition. Real-time RT-PCR was performed to detect gene expression levels of (A) IL4 and IL10 , (B) MMP9 and TIMP1 , and (C) CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (D) The expression protein of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL4, interleukin 4; IL10, interleukin 10; MMP9, matrix metalloproteinase 9; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane; LPS, lipopolysaccharide.

Article Snippet: CXCL12 protein in conditioned medium was measured by Human CXCL12/SDF-1α ELISA Kit (Quantikine, R&D systems.

Techniques: Quantitative RT-PCR, Gene Expression, Expressing, Control, Comparison, Enzyme-linked Immunosorbent Assay, Standard Deviation

Mitogen-activated protein kinase (MAPK) pathway regulated substrate stiffness-induced CXCL12 expression in human gingival fibroblasts (HGFs). (A) Real-time RT-PCR was performed to detect gene expression levels of CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (B) The protein expression of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests. ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells

doi: 10.3389/fbioe.2026.1753774

Figure Lengend Snippet: Mitogen-activated protein kinase (MAPK) pathway regulated substrate stiffness-induced CXCL12 expression in human gingival fibroblasts (HGFs). (A) Real-time RT-PCR was performed to detect gene expression levels of CXCL12 . The expression of GAPDH was used as an internal control. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). (B) The protein expression of CXCL12 was detected by ELISA analysis. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests. ( n = 4: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. CXCL12, CXC motif chemokine 12; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Article Snippet: CXCL12 protein in conditioned medium was measured by Human CXCL12/SDF-1α ELISA Kit (Quantikine, R&D systems.

Techniques: Expressing, Quantitative RT-PCR, Gene Expression, Control, Comparison, Enzyme-linked Immunosorbent Assay, Standard Deviation

Effects of conditioned media of human gingival fibroblasts (HGF-CM) under different substrate stiffness on human periodontal ligament cells’ behaviors. (A) Human periodontal ligament cells (HPDLCs) cultured with HGF-CM in osteogenic medium for 24 h. HPDLCs morphology was demonstrated using a phase-contrast microscope. Scale bars: 300 μm. (B) Real-time RT-PCR was performed to detect gene expression levels of CXCR4 , which is receptor of CXCL12. (C) Real-time RT-PCR was performed to detect gene expression levels of pro-inflammatory cytokine, IL1b . (D) Real-time RT-PCR was performed to detect gene expression levels of MMP8 and TIMP1 . The expression of GAPDH was used as an internal control. (E) Immunofluorescence analysis was performed to detect the protein expression of CXCR4 (green). The cytoskeleton (F-actin; red) and nuclei (blue) were stained using rhodamine-phalloidin and DAPI, respectively. Scale bars: 50 μm. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL1B, interleukin-1β; MMP8, matrix metalloproteinase 8; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCR4, CXC motif receptor type 4; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells

doi: 10.3389/fbioe.2026.1753774

Figure Lengend Snippet: Effects of conditioned media of human gingival fibroblasts (HGF-CM) under different substrate stiffness on human periodontal ligament cells’ behaviors. (A) Human periodontal ligament cells (HPDLCs) cultured with HGF-CM in osteogenic medium for 24 h. HPDLCs morphology was demonstrated using a phase-contrast microscope. Scale bars: 300 μm. (B) Real-time RT-PCR was performed to detect gene expression levels of CXCR4 , which is receptor of CXCL12. (C) Real-time RT-PCR was performed to detect gene expression levels of pro-inflammatory cytokine, IL1b . (D) Real-time RT-PCR was performed to detect gene expression levels of MMP8 and TIMP1 . The expression of GAPDH was used as an internal control. (E) Immunofluorescence analysis was performed to detect the protein expression of CXCR4 (green). The cytoskeleton (F-actin; red) and nuclei (blue) were stained using rhodamine-phalloidin and DAPI, respectively. Scale bars: 50 μm. Data were statistically analyzed by one-way ANOVA followed by Tukey’s multiple comparison tests ( n = 3: P < 0.05). Data are presented as the mean ± standard deviation (SD), with different letters indicating statistically significant differences between multiple groups. IL1B, interleukin-1β; MMP8, matrix metalloproteinase 8; TIMP1, tissue inhibitor of matrix metalloproteinases 1; CXCR4, CXC motif receptor type 4; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PDMS, polydimethylsiloxane.

Article Snippet: CXCL12 protein in conditioned medium was measured by Human CXCL12/SDF-1α ELISA Kit (Quantikine, R&D systems.

Techniques: Cell Culture, Microscopy, Quantitative RT-PCR, Gene Expression, Expressing, Control, Immunofluorescence, Staining, Comparison, Standard Deviation

Schematic illustration shows the role of human gingival fibroblast–conditioned media (HGF-CM) in regulating osteogenic differentiation of human periodontal ligament cells (HPDLCs). (A) ECM stiffness stimulates CXCL12 chemokine expression in HGFs, which is associated with enhanced osteogenic responses in HPDLCs. (B) A potential clinical application of this mechanism is the utilization of HGF-derived factors to suppress inflammatory bone resorption and stabilize periodontal tissues. CXCL12: CXC motif chemokine 12.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells

doi: 10.3389/fbioe.2026.1753774

Figure Lengend Snippet: Schematic illustration shows the role of human gingival fibroblast–conditioned media (HGF-CM) in regulating osteogenic differentiation of human periodontal ligament cells (HPDLCs). (A) ECM stiffness stimulates CXCL12 chemokine expression in HGFs, which is associated with enhanced osteogenic responses in HPDLCs. (B) A potential clinical application of this mechanism is the utilization of HGF-derived factors to suppress inflammatory bone resorption and stabilize periodontal tissues. CXCL12: CXC motif chemokine 12.

Article Snippet: CXCL12 protein in conditioned medium was measured by Human CXCL12/SDF-1α ELISA Kit (Quantikine, R&D systems.

Techniques: Expressing, Derivative Assay

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