LIMCH1

Last update 08 May 2025

Basic Info

Synonyms

DKFZP686A01247, KIAA1102, LIM and calponin homology domains 1

+ [4]

Introduction

Actin stress fibers-associated protein that activates non-muscle myosin IIa. Activates the non-muscle myosin IIa complex by promoting the phosphorylation of its regulatory subunit MRLC/MYL9. Through the activation of non-muscle myosin IIa, positively regulates actin stress fibers assembly and stabilizes focal adhesions. It therefore negatively regulates cell spreading and cell migration.

100 Clinical Results associated with LIMCH1

100 Translational Medicine associated with LIMCH1

0 Patents (Medical) associated with LIMCH1

Literatures (Medical) associated with LIMCH1

01 May 2025·Arteriosclerosis, Thrombosis, and Vascular Biology

The 9p21.3 Coronary Artery Disease Risk Locus Drives Vascular Smooth Muscle Cells to an Osteochondrogenic State

Article

Author: Miller, Clint L. ; Suryavanshi, Shraddha ; Zade, Rohan ; Lo Sardo, Valentina ; Parikh, Parth ; de Medeiros Vieira, Carolina ; Mosquera, Jose Verdezoto ; Salido, Elsa

BACKGROUND:Genome-wide association studies have identified common genetic variants at ≈300 human genomic loci linked to coronary artery disease susceptibility. Among these genomic regions, the most impactful is the 9p21.3 coronary artery disease risk locus, which spans a 60-kb gene desert and encompasses ≈80 SNPs (single nucleotide polymorphism) in high linkage disequilibrium. Despite ≈2 decades since its discovery, the role of the 9p21.3 locus in cells of the vasculature remains incompletely resolved.METHODS: We differentiated induced pluripotent stem cells (iPSCs) from risk, nonrisk donors at 9p21.3, and isogenic knockouts into vascular smooth muscle cells (VSMCs). We performed single-cell transcriptomic profiling, including coembedding and comparison with publicly available human arterial data sets. We conducted functional characterization using migration and calcification assays and confirmed our findings on iPSC–VSMCs derived from additional donors. Finally, we used overexpression of ANRIL followed by gene expression analysis. RESULTS: We demonstrated that iPSC–VSMCs harboring the 9p21.3 risk haplotype preferentially adopt an osteochondrogenic state and show remarkable similarity to fibrochondrocytes from human artery tissue. The transcriptional profile and functional assessment of migration and calcification capacity across iPSC–VSMC lines from multiple donors concordantly resemble an osteochondrogenic state. Importantly, we identified numerous transcription factors driving different VSMC state trajectories. Additionally, we prioritized LIMCH1 and CRABP1 as signature genes critical for defining the risk transcriptional program. Finally, overexpression of a short isoform of ANRIL in 9p21.3 knockout cells was sufficient to induce the osteochondrogenic transcriptional signature. CONCLUSIONS: Our study provides new insights into the mechanism of the 9p21.3 risk locus and defines its previously undescribed role in driving a disease-prone transcriptional and functional state in VSMCs concordant with an osteochondrogenic-like state. Our data suggest that the 9p21.3 risk haplotype likely promotes arterial calcification, through altered expression of ANRIL , in a cell type–specific and cell-autonomous manner, providing insight into potential risk assessment and treatment for carriers.

18 Feb 2025·Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences

[LIM and calponin homology domains 1 may function as promising biological markers to aid in the prognostic prediction of oral squamous cell carcinoma].

Article

Author: Li, Yuehua ; Shen, Yajun ; Cai, Zhigang ; Shan, Xiaofeng ; Xu, Li ; Xie, Shang ; Shi, Wen

OBJECTIVETo explore the function of LIM and calponin homology domains 1 (LIMCH1) in the development and progression of oral squamous cell carcinoma (OSCC), along with their potential clinical applications.METHODSBy utilizing transcriptome sequencing data from two groups of oral squamous cell carcinoma patients, along with bioinformatics analytical techniques such as Gene Ontology (GO) and gene co-expression networks, we identified genes that might play a pivotal role in the pathogenesis of oral squamous cell carcinoma. We employed real-time quantitative PCR and Western blotting to validate the expression patterns of these genes across twelve patient tissue samples. Furthermore, we conducted CCK-8 assays, flow cytometry analyses, and scratch wound healing assays to assess the impact of key genes on the biological behaviors of both the Cal27 oral squamous cell carcinoma cell line and the potentially malignant DOK oral lesion cell line. Additionally, we examined correlations between these key genes and clinical disease parameters in 214 oral squamous cell carcinoma patients using The Cancer Genome Atlas (TCGA) data; gene set enrichment analysis (GSEA) analysis results were also incorporated to enhance our findings from real-time quantitative PCR and Western blotting regarding potential mechanisms underlying the action of these key genes.RESULTSThe integrated analysis of sequencing data and bioinformatics revealed that LIMCH1 exhibited significantly reduced mRNA (P < 0.001) and protein levels (P < 0.01) in the oral squamous cell carcinoma tissues compared with normal control tissues. In the Cal27 cells, the low LIMCH1 level group demonstrated a larger wound healing area within 24 hours than the control group (P < 0.01), enhanced proliferation capacity over 72 hours relative to the control group (P < 0.01), and an increased apoptosis rate within 24 hours compared with the high expression group (P < 0.05). However, no significant differences were observed between the low and high level groups in DOK cells. Furthermore, it was determined that low LIMCH1 level correlated with poor prognosis in the patients (P=0.013) and a higher lymph node metastasis rate (P < 0.05). Investigations into the potential mechanisms of action indicated that LIMCH1 did not influence the onset or progression of oral squamous cell carcinoma via the epithelial-mesenchymal transition pathway.CONCLUSIONLIMCH1 level may function as a promising biomarker to aid in the prognostic assessment of oral squamous cell carcinoma; however, its precise mechanistic role requires further investigation.

01 Jan 2025·International Journal of Hygiene and Environmental Health

Associations between metal/metalloid exposure during pregnancy and placental growth characteristics: Findings from the Hangzhou birth cohort study II

Article

Author: Zhou, Jiena ; Zhong, Kunhong ; Tang, Jun ; Huang, Kegui ; Luo, Qiong ; Xu, Yang ; Jin, Lanfei ; Zhao, Hao ; Chen, Guangdi ; Zhu, Qinheng ; Zhang, Dan ; Zhou, Yexinyi ; Guo, Jing

Previous studies have suggested that metal/metalloid (hereafter referred to as metal) exposure may influence placental growth by affecting gene expression in the placenta. However, no epidemiological studies have been conducted to validate the relationships between metals exposure, placental gene expression, and placental growth at the population level. This study aims to investigate these relationships based on Hangzhou birth cohort study II (HBCS-II). Totally, 1025 participants were derived from HBCS-II. Thirteen metals levels in the placenta were measured using inductively coupled plasma mass spectrometry. Placental growth characteristics were assessed, including placental weight, chorionic disc area, placental eccentricity, and distance from cord insertion site to the nearest edge of placenta (DCIEP). The relationships between metals exposure and placental growth characteristics were examined using the elastic net model combined unpenalized linear regression model. Placental gene expression levels were analyzed through RNA sequencing and real-time polymerase chain reaction (RT-qPCR), and mediation analysis was conducted to investigate whether placental gene expression could mediate the relationship between metal exposure and placental growth. Notably, the results showed that a unite increase in Ln-transformed cadmium (Cd) levels was associated with a reduction of 16.4 g [95% confidence interval (CI): 31.2, -1.5] in placental weight, 13.9 cm² (95%CI: 20.0, -7.8) in chorionic disc area, and 0.3 cm (95%CI: 0.55, -0.06) in DCIEP. Through RNA sequencing followed by validation, significant associations were observed between placental Cd level and increased expression of placental genes, including TNFAIP2, OLAH, FLT4, SH3PXD2A, LIMCH1, BCL6, SLCO2A1, and CPSF1. Additionally, increased placental TNFAIP2, OLAH, FLT4, SH3PXD2A and LIMCH1 expression was linked to reduced placental weight. Moreover, SH3PXD2A was associated with decreased chorionic disc area. Mediation analysis showed that placental Cd level was associated with a 12.0 g (95%CI: 23.8, -2.7) decrease in placental weight mediated through the upregulation of FTL4 gene expression. The study provides evidence of the association between placental Cd exposure and decreased placental weight, and the FLT4 gene may play a mediating role in this relationship. Future experiment studies should be performed to validate the results.

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LIMCH1

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