Lysyl Oxidase
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2021 ◽  
Vol 16 (10) ◽  
pp. S919
Author(s):  
Y. Chen ◽  
S. Yao ◽  
X. Han ◽  
X. Tong ◽  
Z. Qin ◽  
...  

2021 ◽  
Author(s):  
Rui Dong ◽  
Chun Luo ◽  
Bingyang Li ◽  
Chongyu Hu ◽  
Junyu Liu ◽  
...  

Abstract Introduction: aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease caused by intracranial aneurysm (IA) rupture. Lysyl oxidase (LOX) family genes (LOX-like [LOXL] 1–4) have roles in collagen cross-linking in the extracellular matrix and may be associated with IA rupture. We aimed to explore the association between LOX polymorphisms and the risk of aSAH. Methods This case-control study included two cohorts: 133 and 115 single ruptured and unruptured IA patients, and 65 and 71 multiple ruptured and unruptured IAs patients, respectively. Genotyping of 27 single nucleotide polymorphisms (SNPs) in LOX was performed. Logistic regression analysis was performed to calculate the odds ratios (OR) and 95% confidence intervals (CI) of the SNPs of LOX and risk of aSAH. Results LOX rs180044 and LOXL4 rs3793692 were positively associated with the risk of single IA rupture in the recessive model (OR = 5.66, 2.06; 95% CI = 1.22–26.24, 1.11–3.82, respectively) and LOX rs10519694 demonstrated a protective effect on single IA rupture (dominant model: OR = 0.42, 95% CI = 0.21–0.83; recessive model: OR = 0.16, 95% CI = 0.04–0.65; additive model: OR = 0.46, 95% CI = 0.28–0.78). LOXL1 rs2165241, LOXL2 rs1063582, and LOXL3 rs17010021 demonstrated risk effects on multiple IAs rupture. LOXL3 rs17010022 showed a protective effect on multiple IAs rupture (dominant model: OR = 0.41, 95% CI = 0.21–0.82; additive model: OR = 0.51, 95% CI = 0.30–0.85). Discussion LOX and LOXL4 may be susceptible to single IA rupture, whereas LOXL1-3 may have a role in susceptibility to multiple IAs rupture in the Chinese population, suggesting LOX family genes may associated with aSAH.


2021 ◽  
pp. 153537022110420
Author(s):  
Qing Chu ◽  
Ying Xiao ◽  
Xin Song ◽  
Y James Kang

A significant amount of cardiomyocytes in subendocardial region survive from ischemic insults. In order to understand the mechanism by which these cardiomyocytes survive, the present study was undertaken to examine changes in these surviving cardiomyocytes and their extracellular matrix. Male C57BL/6 mice aged 8–12 weeks old were subjected to a permanent left anterior descending coronary artery ligation to induce ischemic injury. The hearts were collected at 1, 4, 7, or 28 days after the surgery and examined by histology. At day 1 after left anterior descending ligation, there was a significant loss of cardiomyocytes through apoptosis, but a proportion of cardiomyocytes were surviving in the subendocardial region. The surviving cardiomyocytes were gradually changed from rod-shaped to round-shaped, and appeared disconnected. Connexin 43, an important gap junction protein, was significantly decreased, and collagen I and III deposition was significantly increased in the extracellular matrix. Furthermore, lysyl oxidase, a copper-dependent amine oxidase catalyzing the cross-linking of collagens, was significantly increased in the extracellular matrix, paralleled with the surviving cardiomyocytes. Inhibition of lysyl oxidase activity reduced the number of surviving cardiomyocytes. Thus, the extracellular matrix remodeling is correlated with the deformation of cardiomyocytes, and the electrical disconnection between the surviving cardiomyocytes due to connexin 43 depletion and the increase in lysyl oxidase would help these deformed cardiomyocytes survive under ischemic conditions.


2021 ◽  
Vol 11 (9) ◽  
Author(s):  
An Huang ◽  
Yi‐Shiuan Lin ◽  
Ling‐Zhen Kao ◽  
Yu‐Wei Chiou ◽  
Gang‐Hui Lee ◽  
...  
Keyword(s):  

2021 ◽  
Vol 35 (9) ◽  
Author(s):  
Hagar Grunwald ◽  
Kristina L. Hunker ◽  
Isabelle Birt ◽  
Rohtem Aviram ◽  
Shelly Zaffryar‐Eilot ◽  
...  

2021 ◽  
Vol 22 (8) ◽  
pp. 2493-2499
Author(s):  
Sanjit Mukherjee ◽  
Atul Katarkar ◽  
Richa Dhariwal ◽  
Sweta Mohanty ◽  
Basudev Mahato ◽  
...  

2021 ◽  
Vol 22 (15) ◽  
pp. 8072
Author(s):  
Talita de S. Laurentino ◽  
Roseli da S. Soares ◽  
Antonio M. Lerario ◽  
Suely K. N. Marie ◽  
Sueli M. Oba-Shinjo

Lysyl oxidase-like 3 (LOXL3), belonging to the lysyl oxidase family, is responsible for the crosslinking in collagen or elastin. The cellular localization of LOXL3 is in the extracellular space by reason of its canonical function. In tumors, the presence of LOXL3 has been associated with genomic stability, cell proliferation, and metastasis. In silico analysis has shown that glioblastoma was among tumors with the highest LOXL3 expression levels. LOXL3 silencing of U87MG cells by siRNA led to the spreading of the tumor cell surface, and the transcriptome analysis of these cells revealed an upregulation of genes coding for extracellular matrix, cell adhesion, and cytoskeleton components, convergent to an increase in cell adhesion and a decrease in cell invasion observed in functional assays. Significant correlations of LOXL3 expression with genes coding for tubulins were observed in the mesenchymal subtype in the TCGA RNA-seq dataset of glioblastoma (GBM). Conversely, genes involved in endocytosis and lysosome formation, along with MAPK-binding proteins related to focal adhesion turnover, were downregulated, which may corroborate the observed decrease in cell viability and increase in the rate of cell death. Invasiveness is a major determinant of the recurrence and poor outcome of GBM patients, and downregulation of LOXL3 may contribute to halting the tumor cell invasion.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chun Luo ◽  
Chongyu Hu ◽  
Bingyang Li ◽  
Junyu Liu ◽  
Liming Hu ◽  
...  

PurposeIntracranial aneurysms (IA) comprise a multifactorial disease with unclear physiological mechanisms. The lysyl oxidase (LOX) family genes (LOX, LOX–like 1–4) plays important roles in extracellular matrix (ECM) reconstruction and has been investigated in terms of susceptibility to IA in a few populations. We aimed to determine whether polymorphisms in LOX family genes are associated with susceptibility to IA in a Chinese population.MethodsThis case-control study included 384 patients with IA and 384 healthy individuals without IA (controls). We genotyped 27 single nucleotide polymorphisms (SNPs) of LOX family genes using the Sequenom MassARRAY® platform. These SNPs were adjusted for known risk factors and then, odds ratios (OR) and 95% confidence intervals (CI) were evaluated using binary logistic regression analysis.ResultsThe result showed that LOX rs10519694 was associated with the risk of IA in recessive (OR, 3.88; 95% CI, 1.12–13.47) and additive (OR, 1.56; 95%CI, 1.05–2.34) models. Stratified analyses illustrated that LOX rs10519694 was associated with the risk of single IA in the recessive (OR, 3.95; 95%CI, 1.04–15.11) and additive (OR, 1.64; 95%CI, 1.04–2.56) models. The LOXL2 rs1010156 polymorphism was associated with multiple IA in the dominant model (OR, 1.92; 95%CI, 1.02–3.62). No associations were observed between SNPs of LOXL1, LOXL3, and LOXL4 and risk of IA.ConclusionLOX and LOXL2 polymorphisms were associated with risk of single IA and multiple IA in a Chinese population, suggesting potential roles of these genes in IA. The effects of these genes on IA require further investigation.


2021 ◽  
Author(s):  
Shahan Mamoor

Epithelial ovarian cancer (EOC) is the most lethal gynecologic cancer (1). We performed discovery of genes associated with epithelial ovarian cancer and of the high-grade serous ovarian cancer (HGSC) subtype, using published microarray data (2, 3) to compare global gene expression profiles of normal ovary or fallopian tube with that of primary tumors from women diagnosed with epithelial ovarian cancer or HGSC. We identified the gene encoding lysyl oxidase, LOX, as among the genes whose expression was most different in epithelial ovarian cancer as compared to the normal fallopian tube. LOX expression was significantly higher in high-grade serous ovarian tumors relative to normal fallopian tube. LOX expression correlated with overall survival in patients with ovarian cancer. These data indicate that expression of LOX is perturbed in epithelial ovarian cancers broadly and in ovarian cancers of the HGSC subtype. LOX may be relevant to pathways underlying ovarian cancer initiation (transformation) or progression.


Author(s):  
Mengxia Ying ◽  
Yan Chen ◽  
Bo Yuan

Background: The excessive healing response during wound repair can result in hypertrophic scars (HS). Lysyl oxidase like 1 (LOXL1) has been reported to be associated with fibrosis via targeting TGF-β1 signaling. This study aimed to investigate the effect of LOXL1 on HS formation. Methods: The expression of LOXL1 in HS tissues and TGF-β1-induced HSFs was detected via RT-qPCR and western blot. LOXL1 was silenced in HSFs using transfection with short hairpin RNA (shRNA), then wound healing process including cell proliferation, cell cycle distribution, migration and extracellular matrix deposition along with Smad expression were measured by CCK-8, EdU staining, flow cytometry, transwell, immunofluorescence and western blot assays. Results: LOXL1 was up-regulated in HS tissues and TGF-β1-induced HSFs. Knockdown of LOXL1 inhibited proliferation and migration, but promoted cell cycle G0/G1 phase arrest in TGF-β1-induced HSFs. The increased expression of cyclin D1, CDK4, MMP2, MMP9, COL1A1, COL1A2, fibronectin, COL3A1, α-SMA, but decreased expression of p27, and the phosphorylation of Smad2 and Smad3 caused by TGF-β1 were also blocked by LOXL1 silence. Conclusions: Silence of LOXL1 could effectively inhibit TGF-β1-induced proliferation, migration and ECM deposition in HSFs via inactivating Smad pathway. Targeting LOXL1 may have future therapeutic implications for HS treatment.


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