Spinal cord injury (SCI) continues to result in high morbidity and mortality throughout the world. An effective neuroprotective agent is still not available to counteract secondary damage caused by traumatic injury. Thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) have a role in angiogenesis, scar deposition, inflammation and may affect astrocyte phenotype and mobility. We investigated the role of TSP-1 and TGF-beta in a model of spinal cord injury in rats. Forty female Sprague-Dawley rats were randomly divided into two equal groups: the experimental group was subject to SCI using an impactor and the sham-operated group was not subject to SCI. These animals were sacrificed at 12 h and 24 h after SCI for immunochemistry and Western blot analysis of the injured spinal segment for the expression of the TSP-1 and TGF-beta proteins. We found that TSP-1 and TGF-beta expression increased immediately after SCI in the injured segment. After 12 h, TSP-1 concentrations increased more rapidly and dramatically than TGF-beta in the injured segment of the spinal cord. Elevations in TSP-1 and TGF-beta concentrations persisted for 24 h after injury. These results show that elevated expression of TSP-1 and TGF-beta can be detected in the injured segment of the spinal cord 12 and 24 h after injury. Thus, TSP-1 and TGF-beta may have a role in SCI.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jocn.2008.09.014 | DOI Listing |
Cardiovasc Ther
January 2025
Department of Biomedical Sciences, Joan C. Edwards School of Medicine at Marshall University, Huntington, West Virginia, USA.
Thymidine phosphorylase (TYMP) promotes platelet activation and thrombosis while suppressing vascular smooth muscle cell (VSMC) proliferation. Both processes are central to the development and progression of abdominal aortic aneurysms (AAAs). We hypothesize that TYMP plays a role in AAA development.
View Article and Find Full Text PDFGut
October 2024
Department of Medicine II, University Medical Center Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany
Objective: Extracellular matrix protein 1 (ECM1) serves as a gatekeeper of hepatic fibrosis by maintaining transforming growth factor-β1 (TGF-β1) in its latent form. ECM1 knockout (KO) causes latent (L) TGF-β1 activation, resulting in hepatic fibrosis with rapid mortality. In chronic liver disease (CLD), ECM1 decreases with increasing CLD severity.
View Article and Find Full Text PDFPLoS One
October 2024
Department of Life Science, Biomedi Campus, Dongguk University-Seoul, Goyang-si, Gyeonggi-do, Korea.
Pulmonary fibrosis is characterized by excessive extracellular matrix (ECM) accumulation caused by detrimental stimuli. The progressive impairment in lung functions is chronic and highly fatal, presenting itself as a global health challenge. Because of the lack of efficacious treatments, the underlying mechanism should be investigated.
View Article and Find Full Text PDFCancer Res
January 2025
MOE Key Laboratory of Gene Function and Regulation, Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, School of Life Sciences, State Key Laboratory of Oncology in South China, Sun Yat-sen University, Guangzhou, P. R. China.
Emerging evidence suggests that TGFβ1 can inhibit angiogenesis, contradicting the coexistence of active angiogenesis and high abundance of TGFβ1 in the tumor microenvironment. Here, we investigated how tumors overcome the antiangiogenic effect of TGFβ1. TGFβ1 treatment suppressed physiologic angiogenesis in chick chorioallantoic membrane and zebrafish models but did not affect angiogenesis in mouse hepatoma xenografts.
View Article and Find Full Text PDFWorld J Mens Health
August 2024
Department of Urology, Peking University First Hospital, Beijing, China.
Purpose: To examine the role and mechanism of thrombospondin-1 (TSP1) in the development of fibrosis in diabetes mellitus-induced erectile dysfunction (DMED).
Materials And Methods: DMED was induced by intraperitoneal streptozotocin injection. All rats were categorized into three groups: control group (n=8), DMED group (n=8) and DMED+Leu-Ser-Lys-Leu (LSKL) group (n=8).
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!