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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 127 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 127 article reviews

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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

CCDC80 + fibroblasts recruit effector CD8 + T cells into the danger zone and drive their exhaustion via CXCL12. a Spatial deconvolution of effector CD8 + T cells (CD8_eff) and exhausted CD8 + T cells (CD8_exhau). b Spatial CellChat analysis of CXCL signaling between CD8 + T cell subsets and CCDC80 + or CCDC80 − fibroblasts. c Bubble plot of ligand-receptor pairs between CD8 + T cell subsets and CCDC80 + or CCDC80 − fibroblasts. d Ligand–receptor interaction analysis showing exclusive engagement of CCDC80 + fibroblasts in CXCL12–CXCR4 signaling with both CD8_eff and CD8_exhau cells. e Quantification of CD8_eff and CD8_exhau recruitment in intestinal-type GC (GC3). f Spatial clustering of GC6 sample. g Pseudotime trajectory from cluster 1 to cluster 0. h Representative trajectory (15 − 10/38/62) demonstrating spatial progression to exhaustion. i qRT-PCR for CCDC80 mRNA expression in NIH-3T3 fibroblasts. j Immunoblot for CCDC80 protein expression. k qRT-PCR for CXCL12 mRNA in CCDC80-overexpressing fibroblasts. l ELISA for quantification of CXCL12 secretion. m Schematic of fibroblast-CD8 + T cell co-culture experiment. n Flow cytometry for PD-1 expression on CD8 + T cells with or without CXCL12 blockade. o Flow cytometry for TIM-3 expression on CD8 + T cells with or without CXCL12 blockade

Journal: Apoptosis

Article Title: Spatially defined danger zone shapes gastric cancer progression through CCDC80 + fibroblast–induced CD8 + T cell dysfunction

doi: 10.1007/s10495-026-02287-1

Figure Lengend Snippet: CCDC80 + fibroblasts recruit effector CD8 + T cells into the danger zone and drive their exhaustion via CXCL12. a Spatial deconvolution of effector CD8 + T cells (CD8_eff) and exhausted CD8 + T cells (CD8_exhau). b Spatial CellChat analysis of CXCL signaling between CD8 + T cell subsets and CCDC80 + or CCDC80 − fibroblasts. c Bubble plot of ligand-receptor pairs between CD8 + T cell subsets and CCDC80 + or CCDC80 − fibroblasts. d Ligand–receptor interaction analysis showing exclusive engagement of CCDC80 + fibroblasts in CXCL12–CXCR4 signaling with both CD8_eff and CD8_exhau cells. e Quantification of CD8_eff and CD8_exhau recruitment in intestinal-type GC (GC3). f Spatial clustering of GC6 sample. g Pseudotime trajectory from cluster 1 to cluster 0. h Representative trajectory (15 − 10/38/62) demonstrating spatial progression to exhaustion. i qRT-PCR for CCDC80 mRNA expression in NIH-3T3 fibroblasts. j Immunoblot for CCDC80 protein expression. k qRT-PCR for CXCL12 mRNA in CCDC80-overexpressing fibroblasts. l ELISA for quantification of CXCL12 secretion. m Schematic of fibroblast-CD8 + T cell co-culture experiment. n Flow cytometry for PD-1 expression on CD8 + T cells with or without CXCL12 blockade. o Flow cytometry for TIM-3 expression on CD8 + T cells with or without CXCL12 blockade

Article Snippet: The collected supernatant was assayed for CXCL12 using an ELISA kit (Cat# MCX120, R&D Systems, Minneapolis, MN, USA), following the manufacturer’s instructions.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Flow Cytometry

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