ITGA8

Last update 08 May 2025

Basic Info

Synonyms

Integrin alpha-8, Integrin alpha-8 heavy chain, Integrin alpha-8 light chain

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Introduction

Integrin alpha-8/beta-1 functions in the genesis of kidney and probably of other organs by regulating the recruitment of mesenchymal cells into epithelial structures. It recognizes the sequence R-G-D in a wide array of ligands including TNC, FN1, SPP1 TGFB1, TGFB3 and VTN. NPNT is probably its functional ligand in kidney genesis. Neuronal receptor for TNC it mediates cell-cell interactions and regulates neurite outgrowth of sensory and motor neurons.

100 Clinical Results associated with ITGA8

100 Translational Medicine associated with ITGA8

0 Patents (Medical) associated with ITGA8

185

Literatures (Medical) associated with ITGA8

01 Jun 2025·Acta Histochemica

The significance of Itga8 and Vangl2 in kidney development: Insights from yotari mice

Article

Author: Katsuyama, Yu ; Filipović, Natalija ; Gelemanović, Andrea ; Vukojević, Katarina ; Kelam, Nela ; Bajt, Patricija ; Racetin, Anita ; Pavlović, Nikola

The permanent kidney develops from the metanephros through the interaction of the ureteric bud (UB) and metanephric mesenchyme (MM). Congenital anomalies of the kidney and urinary tract (CAKUT) are common prenatal diagnoses, and genetic factors play a critical role in their development. This study explores the involvement of Integrin alpha-8 (Itga8) and Van Gogh-like 2 (Vangl2) proteins in kidney development, using the yotari (yot) mouse model, which harbors a mutation in the Dab1 gene, disrupting Reelin signaling. Immunofluorescence was employed to analyze the spatiotemporal expression patterns of these proteins in embryonic and postnatal kidney samples. Our results show that Itga8 and Vangl2 expression is significantly higher in the embryonic kidneys of yot mice than those of wt mice. However, the two groups observed no significant differences in the temporal expression of these proteins in postnatal kidneys. Spatially, Itga8 was most strongly expressed in the metanephric mesenchyme and renal vesicles/immature glomeruli. At the same time, Vangl2 showed the highest expression in the metanephric mesenchyme, renal vesicles/immature glomeruli, and collecting ducts in yot mice. Our findings suggest that the Dab1 mutation disrupts the expression of Itga8 and Vangl2, contributing to kidney developmental defects associated with CAKUT phenotypesThis increased expression suggests a disruption in the normal regulation of these proteins, likely due to the Dab1 mutation, which impairs Reelin signaling. Still, the exact mechanism through which the Reelin/Dab1 pathway influences the expression of examined markers remains to be elucidated. These results offer valuable insights into the factors associated with kidney malformations and suggest potential therapeutic targets for CAKUT abnormalities.

01 May 2025·Acta Pharmacologica Sinica

Genome-wide CRISPR-Cas9 screening identifies ITGA8 responsible for abivertinib sensitivity in lung adenocarcinoma

Article

Author: Chen, Jun ; Zhao, Wen-Hao ; Liu, Ming-Hui ; Ding, Chen ; Chen, Yu-Hao ; Li, Yong-Wen ; Hu, Zi-Xuan ; Chen, Pei-Jie ; Li, Xuan-Guang ; Zhang, Zi-He ; Zhang, Rui-Hao ; Wu, Di ; Liu, Hong-Yu ; Zhu, Guang-Sheng ; Cao, Pei-Jun ; Chen, Chen ; Huang, Hua

The emergence of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) has improved the prognosis for lung cancer patients with EGFR-driven mutations. However, acquired resistance to EGFR-TKIs poses a significant challenge to the treatment. Overcoming the resistance has primarily focused on developing next-generation targeted therapies based on the molecular mechanisms of resistance or inhibiting the activation of bypass pathways to suppress or reverse the resistance. In this study we developed a novel approach by using CRISPR-Cas9 whole-genome library screening to identify the genes that enhance the sensitivity of lung adenocarcinoma cells to EGFR-TKIs. Through this screening, we revealed integrin subunit alpha 8 (ITGA8) as the key gene that enhanced sensitivity to abivertinib in lung adenocarcinoma. Notably, ITGA8 expression was significantly downregulated in lung adenocarcinoma tissues compared to adjacent normal tissues. Bioinformatics analyses revealed that ITGA8 was positively correlated with the sensitivity of lung adenocarcinoma to abivertinib. We showed that knockdown of ITGA8 significantly enhanced the proliferation, migration and invasion of H1975 cells. Conversely, overexpression of ITGA8 reduced the proliferation migration and invasion of H1975/ABIR cells. Furthermore, we demonstrated that ITGA8 sensitized lung adenocarcinoma cells to EGFR-TKIs by attenuating the downstream FAK/SRC/AKT/MAPK signaling pathway. In H1975 cell xenograft mouse models, knockdown of ITGA8 significantly increased tumor growth and reduced the sensitivity to abivertinib, whereas overexpression of ITGA8 markedly suppressed tumor proliferation and enhanced sensitivity to the drug. This study demonstrates that ITGA8 inhibits the proliferation, invasion and migration of lung adenocarcinoma cells, enhances the sensitivity to EGFR-TKIs, improves treatment efficacy, and delays the progression of acquired resistance. Thus, ITGA8 presents a potential therapeutic candidate for addressing acquired resistance to EGFR-TKIs from a novel perspective.

01 Apr 2025·Biochemical and Biophysical Research Communications

ITGA8 deficiency in hepatic stellate cells attenuates CCl4-Induced liver fibrosis via suppression of COL11A1

Article

Author: You, Hong ; Yang, Aiting ; Han, Qi ; Li, Hong ; Yan, Xuzhen ; Zhang, Wen ; Wu, Wenyue ; Chen, Wei ; Wang, Yiwen

BACKGROUND AND OBJECTIVELiver fibrosis is a pathological process driven by chronic liver injury, characterized by excessive extracellular matrix (ECM) deposition due to hepatic stellate cell (HSC) activation. Integrins are critical regulators of ECM remodeling and HSC activation, yet the role of integrin α8(ITGA8) in liver fibrosis remains unclear. This study aims to investigate the function and underlying mechanisms of HSC-derived ITGA8 in liver fibrosis and evaluate the therapeutic potential of ITGA8-targeted intervention.METHODSA CCl₄-induced mouse liver fibrosis model and public database analysis were used to assess ITGA8 expression and localization in liver fibrosis. AAV2/6-shItga8 was utilized to selectively silence HSC-derived ITGA8, and its effects on HSC activation and ECM accumulation were examined. In addition, in vitro ITGA8 knockdown combined with proteomic analysis was performed to explore the molecular mechanisms linking ITGA8 to ECM remodeling.RESULTSITGA8 expression was significantly upregulated in fibrotic liver tissues across different etiologies, with a strong colocalization with HSCs. Silencing ITGA8 using AAV2/6-shItga8 effectively reduced liver fibrosis, as indicated by decreased hepatic inflammation, lower serum ALT levels, reduced inflammatory cell infiltration, and downregulated expression of pro-inflammatory cytokines. Fibrosis markers, including Sirius Red staining, type I collagen deposition, and α-SMA expression, were all reduced upon Itga8 silencing. Proteomic analysis revealed that ITGA8 regulates liver fibrosis through the ECM-receptor interaction pathway, with COL11A1 identified as a key downstream target. ITGA8 knockdown significantly suppressed COL11A1 expression, and reduced HSC-mediated collagen contraction, suggesting that ITGA8 contributes to ECM cross-linking and fibrosis progression via COL11A1 regulation.CONCLUSIONThis study demonstrates that HSC-derived ITGA8 promotes ECM accumulation and liver fibrosis progression by regulating COL11A1. Targeted silencing of ITGA8 via AAV2/6-shItga8 effectively alleviates liver fibrosis, providing new insights into ITGA8 as a potential therapeutic target for antifibrotic treatment.

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ITGA8

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