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OriGene lentiviral particles encoding arid2 silencing

<t>ARID2</t> expression increased over time in BMSCs undergoing osteogenesis, while ARID2 silencing inhibited proliferation and osteogenesis but favored adipogenesis. (A–B) BMSCs were induced to differentiate into osteoblasts and sampled at 1, 3, 5, 7, and 14 days. ARID2 expression was assessed by qRT-PCR (normalized to GAPDH, reference gene) and western blot (normalized to GAPDH, loading control). (C) ARID2 expression in normally cultured BMSCs after lentiviral ARID2 silencing <t>(siARID2)</t> was measured by qRT-PCR (GAPDH reference). (D) BMSC viability after ARID2 silencing was measured by MTT assay. (E–F) After 14 days of osteogenic induction, ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. (G) After 14 days of adipogenic induction, lipid deposition was evaluated by Oil Red O staining (×200, scale bar 50 µm). * P <0.05, *** P <0.001 vs 1 day; ^^ P <0.01, ^^^ P <0.001 vs siNC, n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; ARID2, AT-rich interactive domain–containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative-control lentivirus; OD, optical density.

Lentiviral Particles Encoding Arid2 Silencing, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews

lentiviral particles encoding arid2 silencing - by Bioz Stars, 2026-07

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1) Product Images from "Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management"

Article Title: Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management

Journal: Journal of Musculoskeletal & Neuronal Interactions

doi: 10.22540/JMNI-26-124

ARID2 expression increased over time in BMSCs undergoing osteogenesis, while ARID2 silencing inhibited proliferation and osteogenesis but favored adipogenesis. (A–B) BMSCs were induced to differentiate into osteoblasts and sampled at 1, 3, 5, 7, and 14 days. ARID2 expression was assessed by qRT-PCR (normalized to GAPDH, reference gene) and western blot (normalized to GAPDH, loading control). (C) ARID2 expression in normally cultured BMSCs after lentiviral ARID2 silencing (siARID2) was measured by qRT-PCR (GAPDH reference). (D) BMSC viability after ARID2 silencing was measured by MTT assay. (E–F) After 14 days of osteogenic induction, ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. (G) After 14 days of adipogenic induction, lipid deposition was evaluated by Oil Red O staining (×200, scale bar 50 µm). * P <0.05, *** P <0.001 vs 1 day; ^^ P <0.01, ^^^ P <0.001 vs siNC, n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; ARID2, AT-rich interactive domain–containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative-control lentivirus; OD, optical density.

Figure Legend Snippet: ARID2 expression increased over time in BMSCs undergoing osteogenesis, while ARID2 silencing inhibited proliferation and osteogenesis but favored adipogenesis. (A–B) BMSCs were induced to differentiate into osteoblasts and sampled at 1, 3, 5, 7, and 14 days. ARID2 expression was assessed by qRT-PCR (normalized to GAPDH, reference gene) and western blot (normalized to GAPDH, loading control). (C) ARID2 expression in normally cultured BMSCs after lentiviral ARID2 silencing (siARID2) was measured by qRT-PCR (GAPDH reference). (D) BMSC viability after ARID2 silencing was measured by MTT assay. (E–F) After 14 days of osteogenic induction, ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. (G) After 14 days of adipogenic induction, lipid deposition was evaluated by Oil Red O staining (×200, scale bar 50 µm). * P <0.05, *** P <0.001 vs 1 day; ^^ P <0.01, ^^^ P <0.001 vs siNC, n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; ARID2, AT-rich interactive domain–containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative-control lentivirus; OD, optical density.

Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Control, Cell Culture, MTT Assay, Activity Assay, Staining, Derivative Assay, Reverse Transcription, Negative Control

STK39 overexpression increased ARID2 expression to encourage BMSC proliferation and osteogenesis. (A–B) STK39 and ARID2 expression levels in normally cultured BMSCs after transduction with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39 were assessed by qRT-PCR (normalized to GAPDH). (C) BMSC viability after the indicated transductions was measured by MTT assay. (D–E) BMSCs were transduced as indicated and then subjected to osteogenic induction for 14 days. ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; + P <0.05, +++ P <0.001, + vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; OD, optical density.

Figure Legend Snippet: STK39 overexpression increased ARID2 expression to encourage BMSC proliferation and osteogenesis. (A–B) STK39 and ARID2 expression levels in normally cultured BMSCs after transduction with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39 were assessed by qRT-PCR (normalized to GAPDH). (C) BMSC viability after the indicated transductions was measured by MTT assay. (D–E) BMSCs were transduced as indicated and then subjected to osteogenic induction for 14 days. ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; + P <0.05, +++ P <0.001, + vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; OD, optical density.

Techniques Used: Over Expression, Expressing, Cell Culture, Transduction, Quantitative RT-PCR, MTT Assay, Activity Assay, Staining, Derivative Assay, Reverse Transcription, Negative Control, Plasmid Preparation, Control

STK39 overexpression increased ARID2 expression and restrained NF-κB signaling in BMSCs undertaking osteogenesis. (A-C) BMSCs were transduced with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39, then underwent osteogenic differentiation for 14 days. NF-κB pathway–related proteins were assessed by western blot. p-p65 was normalized to total p65; ARID2 and IκBα were normalized to GAPDH. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; ++ P <0.01, +++ P <0.001 vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; p-p65, phosphorylated p65; NF-κB, nuclear factor κB.

Figure Legend Snippet: STK39 overexpression increased ARID2 expression and restrained NF-κB signaling in BMSCs undertaking osteogenesis. (A-C) BMSCs were transduced with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39, then underwent osteogenic differentiation for 14 days. NF-κB pathway–related proteins were assessed by western blot. p-p65 was normalized to total p65; ARID2 and IκBα were normalized to GAPDH. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; ++ P <0.01, +++ P <0.001 vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; p-p65, phosphorylated p65; NF-κB, nuclear factor κB.

Techniques Used: Over Expression, Expressing, Transduction, Western Blot, Derivative Assay, Negative Control, Plasmid Preparation, Control

Image Search Results

The decidua is rich in COL4A1, OPN and HA. (A, B) Compared the expression of COL4A1 (A) and OPN (B) in endometrium (n=5) and decidua (n=5) by Immunohistochemistry. Scale bar, 100 μm and 50 μm. (C) Compared the expression of HA in endometrium (n=8) and decidua (n=8) by Alcian blue staining assays. Scale bar, 100 μm. (D) The levels of COL4A1, OPN and HA from the culture supernatant of DSCs (n=6) or ESCs (n=6) were evaluated by ELISA. The data are presented as the mean ± SEM; two-tailed Student’s t -test; ** P < 0.01, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: Decidual stromal cells drive CD16 + macrophages towards an immunoregulatory phenotype via extracellular matrix-adhesion molecule interaction during early pregnancy

doi: 10.3389/fimmu.2025.1747323

Figure Lengend Snippet: The decidua is rich in COL4A1, OPN and HA. (A, B) Compared the expression of COL4A1 (A) and OPN (B) in endometrium (n=5) and decidua (n=5) by Immunohistochemistry. Scale bar, 100 μm and 50 μm. (C) Compared the expression of HA in endometrium (n=8) and decidua (n=8) by Alcian blue staining assays. Scale bar, 100 μm. (D) The levels of COL4A1, OPN and HA from the culture supernatant of DSCs (n=6) or ESCs (n=6) were evaluated by ELISA. The data are presented as the mean ± SEM; two-tailed Student’s t -test; ** P < 0.01, **** P < 0.0001.

Article Snippet: Gene silencing plasmid targeting COL4A1 (si COL4A1 )/ SPP1 (si SPP1 ) or control plasmid was from Shanghai Genechem Co., LTD. (China).

Techniques: Expressing, Immunohistochemistry, Staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test

Exogenous COL4A1, OPN and HA promote development of immunomodulatory CD16 + Mφ. (A, B) After 48 hours of stimulation with exogenous COL4A1 (10 ug/mL), OPN (1 ug/mL) or vehicles, the expression levels of CD16 on U937-induced Mφ ( A ; n=5) and the polarization-related molecules CD86, CD209 and CD206 on CD16 - or CD16 + Mφ ( B ; n=5) were detected by flow cytometry. (C, D) After 48 hours of stimulation with exogenous HA (0, 50, 100 μM), the expression levels of CD16 on U937-induced Mφ ( C ; n=4) and CD86, CD209 and CD206 on CD16 - or CD16 + Mφ ( D ; n=4) were detected by flow cytometry. The data are presented as the mean ± SEM; oneway ANOVA test or two-tailed Student’s t-test; *P < 0.05, **P < 0.01, ****P< 0.0001, NS, no significant difference.

Journal: Frontiers in Immunology

Article Title: Decidual stromal cells drive CD16 + macrophages towards an immunoregulatory phenotype via extracellular matrix-adhesion molecule interaction during early pregnancy

doi: 10.3389/fimmu.2025.1747323

Figure Lengend Snippet: Exogenous COL4A1, OPN and HA promote development of immunomodulatory CD16 + Mφ. (A, B) After 48 hours of stimulation with exogenous COL4A1 (10 ug/mL), OPN (1 ug/mL) or vehicles, the expression levels of CD16 on U937-induced Mφ ( A ; n=5) and the polarization-related molecules CD86, CD209 and CD206 on CD16 - or CD16 + Mφ ( B ; n=5) were detected by flow cytometry. (C, D) After 48 hours of stimulation with exogenous HA (0, 50, 100 μM), the expression levels of CD16 on U937-induced Mφ ( C ; n=4) and CD86, CD209 and CD206 on CD16 - or CD16 + Mφ ( D ; n=4) were detected by flow cytometry. The data are presented as the mean ± SEM; oneway ANOVA test or two-tailed Student’s t-test; *P < 0.05, **P < 0.01, ****P< 0.0001, NS, no significant difference.

Article Snippet: Gene silencing plasmid targeting COL4A1 (si COL4A1 )/ SPP1 (si SPP1 ) or control plasmid was from Shanghai Genechem Co., LTD. (China).

Techniques: Expressing, Flow Cytometry, Two Tailed Test

CD16 + Mφ in the co-culture system are suppressed with the inhibition of COL4A1, OPN and HA in DSCs. (A) DSCs were transfected by plasmid of siRNA targeting COL4A1 (si COL4A1 ; n=3), SPP1 (si SPP1 ; n=3) or control plasmids (n=3) for 72 hours and the efficacy was verified by RT-qPCR. (B-D) After co-cultured with COL4A1 -silenced DSCs, SPP1 -silenced DSCs or control DSCs for 48 hours, CD16 expression of U937-induced Mφ ( B, C ; n=4) and the polarization markers (CD86, CD209 and CD206) of CD16 - or CD16 + macrophages ( D ; n=4) were explored by flow cytometry. (E, F) After co-cultured with 4-MU (a hyaluronic Acid synthesis inhibitor, 500 μM) or vehicle treated DSCs for 48 hours, CD16 expression of U937-induced Mφ ( E ; n=6) and the polarization markers of CD16 - or CD16 + macrophages ( F ; n=6) were explored by flow cytometry. The data are presented as the mean ± SEM; oneway ANOVA test or two-tailed Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, ns, NS significant difference.

Journal: Frontiers in Immunology

Article Title: Decidual stromal cells drive CD16 + macrophages towards an immunoregulatory phenotype via extracellular matrix-adhesion molecule interaction during early pregnancy

doi: 10.3389/fimmu.2025.1747323

Figure Lengend Snippet: CD16 + Mφ in the co-culture system are suppressed with the inhibition of COL4A1, OPN and HA in DSCs. (A) DSCs were transfected by plasmid of siRNA targeting COL4A1 (si COL4A1 ; n=3), SPP1 (si SPP1 ; n=3) or control plasmids (n=3) for 72 hours and the efficacy was verified by RT-qPCR. (B-D) After co-cultured with COL4A1 -silenced DSCs, SPP1 -silenced DSCs or control DSCs for 48 hours, CD16 expression of U937-induced Mφ ( B, C ; n=4) and the polarization markers (CD86, CD209 and CD206) of CD16 - or CD16 + macrophages ( D ; n=4) were explored by flow cytometry. (E, F) After co-cultured with 4-MU (a hyaluronic Acid synthesis inhibitor, 500 μM) or vehicle treated DSCs for 48 hours, CD16 expression of U937-induced Mφ ( E ; n=6) and the polarization markers of CD16 - or CD16 + macrophages ( F ; n=6) were explored by flow cytometry. The data are presented as the mean ± SEM; oneway ANOVA test or two-tailed Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, ns, NS significant difference.

Article Snippet: Gene silencing plasmid targeting COL4A1 (si COL4A1 )/ SPP1 (si SPP1 ) or control plasmid was from Shanghai Genechem Co., LTD. (China).

Techniques: Co-Culture Assay, Inhibition, Transfection, Plasmid Preparation, Control, Quantitative RT-PCR, Cell Culture, Expressing, Flow Cytometry, Two Tailed Test

Patients RM exhibit weakened interactions between DSCs and CD16 + dMφ. (A) Compared the expression of COL4A1 in decidua from women with normal pregnancy (NP, n=8) or recurrent miscarriage (RM, n=8) by Immunohistochemistry. Scale bar, 50 μm. (B) Compared the expression of OPN in decidua from women with NP (n=10) or RM (n=10) by Immunohistochemistry. Scale bar, 50 μm. (C) Compared the expression of HA in decidua from women with NP (n=8) or RM (n=8) by Alcian blue staining assays. Scale bar, 50 μm. (D) Levels of CD16, CD86, CD206 and CD209 in CD45 + CD14 + dMφ from women with NP (n=7) or RM (n=7) by flow cytometry assays. The data are presented as the mean ± SEM; two-tailed Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Frontiers in Immunology

Article Title: Decidual stromal cells drive CD16 + macrophages towards an immunoregulatory phenotype via extracellular matrix-adhesion molecule interaction during early pregnancy

doi: 10.3389/fimmu.2025.1747323

Figure Lengend Snippet: Patients RM exhibit weakened interactions between DSCs and CD16 + dMφ. (A) Compared the expression of COL4A1 in decidua from women with normal pregnancy (NP, n=8) or recurrent miscarriage (RM, n=8) by Immunohistochemistry. Scale bar, 50 μm. (B) Compared the expression of OPN in decidua from women with NP (n=10) or RM (n=10) by Immunohistochemistry. Scale bar, 50 μm. (C) Compared the expression of HA in decidua from women with NP (n=8) or RM (n=8) by Alcian blue staining assays. Scale bar, 50 μm. (D) Levels of CD16, CD86, CD206 and CD209 in CD45 + CD14 + dMφ from women with NP (n=7) or RM (n=7) by flow cytometry assays. The data are presented as the mean ± SEM; two-tailed Student’s t -test; * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Gene silencing plasmid targeting COL4A1 (si COL4A1 )/ SPP1 (si SPP1 ) or control plasmid was from Shanghai Genechem Co., LTD. (China).

Techniques: Expressing, Immunohistochemistry, Staining, Flow Cytometry, Two Tailed Test

Journal: Journal of Musculoskeletal & Neuronal Interactions

Article Title: Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management

doi: 10.22540/JMNI-26-124

Figure Lengend Snippet: ARID2 expression increased over time in BMSCs undergoing osteogenesis, while ARID2 silencing inhibited proliferation and osteogenesis but favored adipogenesis. (A–B) BMSCs were induced to differentiate into osteoblasts and sampled at 1, 3, 5, 7, and 14 days. ARID2 expression was assessed by qRT-PCR (normalized to GAPDH, reference gene) and western blot (normalized to GAPDH, loading control). (C) ARID2 expression in normally cultured BMSCs after lentiviral ARID2 silencing (siARID2) was measured by qRT-PCR (GAPDH reference). (D) BMSC viability after ARID2 silencing was measured by MTT assay. (E–F) After 14 days of osteogenic induction, ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. (G) After 14 days of adipogenic induction, lipid deposition was evaluated by Oil Red O staining (×200, scale bar 50 µm). * P <0.05, *** P <0.001 vs 1 day; ^^ P <0.01, ^^^ P <0.001 vs siNC, n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; ARID2, AT-rich interactive domain–containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative-control lentivirus; OD, optical density.

Article Snippet: Lentiviral particles encoding ARID2 silencing (siARID2; TL306601) and STK39 overexpression (RC223981L4V), together with their corresponding negative controls (siNC; TR30023 and NC; PS100093 ), were obtained from OriGene (Rockville, MD, USA).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control, Cell Culture, MTT Assay, Activity Assay, Staining, Derivative Assay, Reverse Transcription, Negative Control

Journal: Journal of Musculoskeletal & Neuronal Interactions

Article Title: Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management

doi: 10.22540/JMNI-26-124

Figure Lengend Snippet: STK39 overexpression increased ARID2 expression to encourage BMSC proliferation and osteogenesis. (A–B) STK39 and ARID2 expression levels in normally cultured BMSCs after transduction with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39 were assessed by qRT-PCR (normalized to GAPDH). (C) BMSC viability after the indicated transductions was measured by MTT assay. (D–E) BMSCs were transduced as indicated and then subjected to osteogenic induction for 14 days. ALP activity (ALP staining; ×200, scale bar 50 µm) and mineralized nodule formation (Alizarin Red S staining; ×200, scale bar 50 µm) were evaluated. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; + P <0.05, +++ P <0.001, + vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; qRT-PCR, quantitative reverse-transcription PCR; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; OD, optical density.

Techniques: Over Expression, Expressing, Cell Culture, Transduction, Quantitative RT-PCR, MTT Assay, Activity Assay, Staining, Derivative Assay, Reverse Transcription, Negative Control, Plasmid Preparation, Control

Journal: Journal of Musculoskeletal & Neuronal Interactions

Article Title: Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management

doi: 10.22540/JMNI-26-124

Figure Lengend Snippet: STK39 overexpression increased ARID2 expression and restrained NF-κB signaling in BMSCs undertaking osteogenesis. (A-C) BMSCs were transduced with lentiviruses silencing ARID2 (siARID2) and/or lentivirus overexpressing STK39, then underwent osteogenic differentiation for 14 days. NF-κB pathway–related proteins were assessed by western blot. p-p65 was normalized to total p65; ARID2 and IκBα were normalized to GAPDH. * P <0.05, ** P <0.01, *** P <0.001 vs NC+siNC; ^ P <0.05, ^^ P <0.01, ^^^ P <0.001 vs NC+siARID2; ++ P <0.01, +++ P <0.001 vs STK39+siNC. n = 3 biological replicates. BMSCs, bone marrow–derived mesenchymal stromal cells; STK39, serine/threonine kinase 39; ARID2, AT-rich interactive domain-containing protein 2; siARID2, lentivirus-mediated ARID2 silencing; siNC, negative control for ARID2-silencing lentivirus; NC, vector control for STK39 overexpression; p-p65, phosphorylated p65; NF-κB, nuclear factor κB.

Techniques: Over Expression, Expressing, Transduction, Western Blot, Derivative Assay, Negative Control, Plasmid Preparation, Control

Protein–protein interaction (PPI) network analysis: A Construction of PPI network using STRING database and Cytoscape for analysis. B - F Identification of central genes using various algorithms: B MCC, C MNC, D Degree, E EPC, and F Stress. G Core genes (LAX1, CSF3R) identified through Venn diagram analysis

Journal: BMC Geriatrics

Article Title: LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway

doi: 10.1186/s12877-025-06865-x

Figure Lengend Snippet: Protein–protein interaction (PPI) network analysis: A Construction of PPI network using STRING database and Cytoscape for analysis. B - F Identification of central genes using various algorithms: B MCC, C MNC, D Degree, E EPC, and F Stress. G Core genes (LAX1, CSF3R) identified through Venn diagram analysis

Article Snippet: Periodontitis-KO group: Periodontitis model cells were induced and transfected with LAX1 silencing siRNA plasmid(LAX1siRNA, Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques:

Gene expression heatmap: A Heatmap of core gene expression in Alzheimer’s disease datasets ( GSE138260 and GSE203206 ). B Heatmap of core gene expression in periodontitis datasets ( GSE53849 and GSE173078 ). C CTD analysis showing core genes (LAX1, CSF3R) associated with diseases such as respiratory diseases, cognitive impairment, dementia, diabetes, and inflammation

Journal: BMC Geriatrics

Article Title: LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway

doi: 10.1186/s12877-025-06865-x

Figure Lengend Snippet: Gene expression heatmap: A Heatmap of core gene expression in Alzheimer’s disease datasets ( GSE138260 and GSE203206 ). B Heatmap of core gene expression in periodontitis datasets ( GSE53849 and GSE173078 ). C CTD analysis showing core genes (LAX1, CSF3R) associated with diseases such as respiratory diseases, cognitive impairment, dementia, diabetes, and inflammation

Article Snippet: Periodontitis-KO group: Periodontitis model cells were induced and transfected with LAX1 silencing siRNA plasmid(LAX1siRNA, Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques: Gene Expression

LAX1 activates the STAT signaling pathway, promoting inflammation and apoptosis in disease models

Journal: BMC Geriatrics

Article Title: LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway

doi: 10.1186/s12877-025-06865-x

Figure Lengend Snippet: LAX1 activates the STAT signaling pathway, promoting inflammation and apoptosis in disease models

Article Snippet: Periodontitis-KO group: Periodontitis model cells were induced and transfected with LAX1 silencing siRNA plasmid(LAX1siRNA, Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques:

LAX1 promotes inflammatory responses in Alzheimer’s disease and periodontitis, as shown by increased pro-inflammatory cytokine expression in cell models

Journal: BMC Geriatrics

Article Title: LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway

doi: 10.1186/s12877-025-06865-x

Figure Lengend Snippet: LAX1 promotes inflammatory responses in Alzheimer’s disease and periodontitis, as shown by increased pro-inflammatory cytokine expression in cell models

Article Snippet: Periodontitis-KO group: Periodontitis model cells were induced and transfected with LAX1 silencing siRNA plasmid(LAX1siRNA, Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques: Expressing

LAX1 promotes cellular apoptosis in Alzheimer’s disease and periodontitis, as evidenced by increased apoptosis-related protein expression in cell models

Journal: BMC Geriatrics

Article Title: LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway

doi: 10.1186/s12877-025-06865-x

Figure Lengend Snippet: LAX1 promotes cellular apoptosis in Alzheimer’s disease and periodontitis, as evidenced by increased apoptosis-related protein expression in cell models

Article Snippet: Periodontitis-KO group: Periodontitis model cells were induced and transfected with LAX1 silencing siRNA plasmid(LAX1siRNA, Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques: Expressing

Baicalin repressed LDHA mRNA viability via IGF2BP3-dependent manner. (A) Several m 6 A key readers were tested by RT-PCR. SCC25 cells were treated by baicalin administration (0 μmol/L, 50 μmol/L). (B) The positive correlation within LDHA expression and IGF2BP3 expression in clinical cohort. (C) The expression of IGF2BP3 in the tumor samples and normal samples. (D) The fluorescence in situ hybridization (FISH) assay revealed the subcellar location of LDHA and IGF2BP3 in SCC25 cells treated by baicalin administration (0 μmol/L, 50 μmol/L). (E) Western blot assay revealed the protein level of LDHA and IGF2BP3 in SCC25 cells with baicalin administration (0 μmol/L, 50 μmol/L). (F) RIP-PCR analysis revealed the molecular interaction within anti-IGF2BP3 antibody and LDHA mRNA with baicalin administration (0 μmol/L, 50 μmol/L). (G, H) RNA decay analysis revealed the LDHA mRNA stability in SCC25 cells with baicalin administration and IGF2BP3 over-expression. * p < 0.05, ** p < 0.01.

Journal: Journal of Advanced Research

Article Title: Baicalin attenuates the immune escape of oral squamous cell carcinoma by reducing lactate accumulation in tumor microenvironment

doi: 10.1016/j.jare.2025.01.021

Figure Lengend Snippet: Baicalin repressed LDHA mRNA viability via IGF2BP3-dependent manner. (A) Several m 6 A key readers were tested by RT-PCR. SCC25 cells were treated by baicalin administration (0 μmol/L, 50 μmol/L). (B) The positive correlation within LDHA expression and IGF2BP3 expression in clinical cohort. (C) The expression of IGF2BP3 in the tumor samples and normal samples. (D) The fluorescence in situ hybridization (FISH) assay revealed the subcellar location of LDHA and IGF2BP3 in SCC25 cells treated by baicalin administration (0 μmol/L, 50 μmol/L). (E) Western blot assay revealed the protein level of LDHA and IGF2BP3 in SCC25 cells with baicalin administration (0 μmol/L, 50 μmol/L). (F) RIP-PCR analysis revealed the molecular interaction within anti-IGF2BP3 antibody and LDHA mRNA with baicalin administration (0 μmol/L, 50 μmol/L). (G, H) RNA decay analysis revealed the LDHA mRNA stability in SCC25 cells with baicalin administration and IGF2BP3 over-expression. * p < 0.05, ** p < 0.01.

Article Snippet: IGF2BP3 silencing plasmids (Genechem, Shanghai).

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Fluorescence, In Situ Hybridization, Western Blot, Over Expression

Baicalin targeted IGF2BP3/LDHA to reduce lactate accumulation and PD-L1 expression. (A) The lactate enrichment was tested in the SSC25 cells with LDHA overexpression (LDHA) transfection, baicalin administration (50 μmol/L), IGF2BP3 overexpression (IGF2BP3) and IGF2BP3 silencing (sh-IGF2BP3). (B) The extracellular acidification pH value was tested in SCC25 cells. (C) The extracellular acidification rate (ECAR) was tested. (D, E) The PD-L1 surface expression was tested by flow cytometry. Mean fluorescence intensity, MFI. * p < 0.05 related to blank group; #p < 0.05, ##p < 0.01 related to LDHA group.

Journal: Journal of Advanced Research

Article Title: Baicalin attenuates the immune escape of oral squamous cell carcinoma by reducing lactate accumulation in tumor microenvironment

doi: 10.1016/j.jare.2025.01.021

Figure Lengend Snippet: Baicalin targeted IGF2BP3/LDHA to reduce lactate accumulation and PD-L1 expression. (A) The lactate enrichment was tested in the SSC25 cells with LDHA overexpression (LDHA) transfection, baicalin administration (50 μmol/L), IGF2BP3 overexpression (IGF2BP3) and IGF2BP3 silencing (sh-IGF2BP3). (B) The extracellular acidification pH value was tested in SCC25 cells. (C) The extracellular acidification rate (ECAR) was tested. (D, E) The PD-L1 surface expression was tested by flow cytometry. Mean fluorescence intensity, MFI. * p < 0.05 related to blank group; #p < 0.05, ##p < 0.01 related to LDHA group.

Article Snippet: IGF2BP3 silencing plasmids (Genechem, Shanghai).

Techniques: Expressing, Over Expression, Transfection, Flow Cytometry, Fluorescence

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