Human TIMP1 ELISA Kit
- Known as:
- Human TIMP1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1687
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Human TIMP1 ELISA Kit
Related genes to: Human TIMP1 ELISA Kit
- Gene:
- TIMP1 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 1
- Previous symbol:
- TIMP, CLGI
- Synonyms:
- EPO
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-26
Related products to: Human TIMP1 ELISA Kit
Related articles to: Human TIMP1 ELISA Kit
- Tissue inhibitor of metalloproteinase 1 (TIMP1) is essential for the development and progression of various cancers and represents a valuable prognostic indicator. - Source: PubMed
Publication date: 2026/06/09
Kang YanLi YaoqiLiu TianxiangZhu ChenglouMa Junfeng - Circulating sex hormone-binding globulin (SHBG) concentrations are lower in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), reflecting its potential role in metabolic liver dysfunction. Our prior studies demonstrated that SHBG can attenuate MASLD by limiting hepatic lipid deposition, partly through suppression of lipogenic pathways, in both cellular and animal models. In the present work, we have examined whether SHBG could protect against development of liver fibrosis. For this purpose, in vitro and in vivo studies were performed. In vitro, we used co-cultures of human hepatocellular carcinoma cell line (HepG2) and human hepatic stellate cell line (LX-2) cells transfected using an SHBG expression vector vs. vehicle and treated with transforming growth factor beta 1 (TGF-β1). For in vivo studies we used wild-type and human transgenic mice developing liver fibrosis induced by carbon tetrachloride (CCl). Our results clearly showed that SHBG overexpression reduced the TGF-β1-induced expression in collagen in LX-2 cells. Moreover, SHBG overexpression reduced the CCl induced liver fibrosis in both male and female mice. Histological examination revealed that transgenic mice had reduced NAS score and decreased collagen accumulation, assessed by Sirious Red staining. In addition, human transgenic mice treated with CCl exhibited lower collagen 1A1 (Col1A1) protein levels when compared with wild-type CCl treated mice. Mechanistically, SHBG attenuated fibrosis primarily through modulation of the TGF-β1/matrix metalloproteinases (MMPs)/tissue inhibitor metalloproteinases 1 (TIMP1) axis, characterized by reduced TGF-β1 levels, increased metalloprotease activity, and decreased TIMP1 levels compared with wild-type CCl treated mice. Notably, female transgenic mice exhibited greater protection against fibrosis than males, indicating a sex-dependent effect likely mediated by differences in sex steroid signaling. Taken together, we demonstrate for the first time that SHBG protects against liver fibrosis by promoting collagen degradation via the TGF-β1/MMPs/TIMP1 pathway. Further research is needed to elucidate the role of sex steroids in the regulation of MMPs and the observed sexual dimorphism. - Source: PubMed
Publication date: 2026/05/28
Álvarez-Guaita AnnaBriansó-Llort LauraCabrera-Serra JuliaFuertes-Rioja LidiaRamos-Pérez LorenaSalcedo-Allende María TeresaHernández CristinaSimó RafaelSelva David M - This study evaluated serum and urinary extracellular matrix (ECM)-related biomarkers in pediatric patients with vesicoureteral reflux (VUR) and their association with disease severity and renal scarring. Children with VUR and control subjects were included. Serum and urinary concentrations of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), CD147, transforming growth factor-β (TGF-β), and monocyte chemoattractant protein-1 (MCP-1) were analyzed, with urinary values normalized to creatinine. Serum MCP-1 levels were higher in patients with VUR ( < 0.001), whereas other serum biomarkers showed no significant differences. Creatinine-normalized urinary TIMP-1 and TGF-β levels were significantly elevated ( = 0.006 and = 0.008, respectively), while CD147 levels were reduced ( = 0.011) in VUR patients. Receiver operating characteristic analysis demonstrated moderate discriminative performance for uTIMP-1/Cr (AUC = 0.74), uTGF-β/Cr (AUC = 0.73), and uCD147/Cr (AUC = 0.72). Higher urinary levels of MMP-9 ( = 0.014), TIMP-1 ( = 0.003), and MCP-1 ( = 0.015) were associated with high-grade VUR and with bilateral renal scarring ( = 0.048, = 0.041, and = 0.025, respectively). These findings suggest that urinary ECM-related biomarkers may reflect intrarenal inflammatory and fibrotic processes in VUR. However, their clinical applicability remains limited and requires validation in larger, longitudinal studies. - Source: PubMed
Publication date: 2026/05/27
Ratković-Janković MarijaBašić JelenaJevtović-Stoimenov TatjanaGolubović EmilijaPejčić LjiljanaNikolić IvanaBjelaković Bojko - Fibrosis in Crohn's Disease (CD) occurs when there is continuous inflammation and repair mechanisms, which may lead to fibrotic strictures and ultimately intestinal surgical resection. There are limited non-invasive biomarkers for monitoring CD activity, particularly for detecting fibrosis. Thus, we set out to identify biomarkers that could be monitored for the detection and treatment of fibrosis. We used multiplex protein arrays to examine cytokines and pro-fibrotic factors in the serum of CD patients and analyzed their reliability to predict fibrosis. These markers were confirmed in tissues and the role of cytokines in upregulating fibrotic factors was examined. Collagen 1A1, Fibronectin, MMP9, and Timp-1 in patient serum were identified as strong predictors of fibrosis. IL-1β, MCP-1 and TNFα were identified as major regulators of fibrosis factors in human tissues. Overall, we identified four serum markers that are strong indicators of fibrosis and provided some novel insight into the impact of cytokines on fibrotic factors. Taken together, these findings may lead to earlier detection of fibrosis, and improved monitoring and treatment for CD patients. - Source: PubMed
Publication date: 2026/05/31
Abomhya AhmedPanganiban RonaldoHassan Syed AdeelPhinney Brandon BMcAninch StevenYochum GregoryPinchuk Irina VBarrett TerrenceBeswick Ellen J - Despite effective combination antiretroviral therapy (cART), executive function impairment remains prevalent among people living with HIV (PLWH). The pathogenesis of HIV-associated neurocognitive disorder is multifactorial, involving chronic immune activation, metabolic alterations, and neuroinflammatory processes. Matrix metalloproteinases and their tissue inhibitors (TIMPs) contribute to neuroinflammation and blood-brain barrier disruption, but their relationship with executive dysfunction in HIV remains unclear. - Source: PubMed
Publication date: 2026/06/03
Weng Ya-WeiTsai Hung-ChinLee Susan Shin-JungHsu Chih-HuiLin Sheng-Hsiang