4 results match your criteria: "Wujin People's Hospital of Changzhou[Affiliation]"
PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation.
Biosci Rep
July 2019
Department of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China
Myocardial ischemia-reperfusion (I/R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. How to ensure the recovery of blood supply to ischemic myocardial tissue while avoiding or reducing I/R injury remains a critical problem in clinical practice. In the present study, we examined the function of phospholipase C ϵ-1 (PLCE1) by an H9c2 H/R (H/R, hypoxia-reoxygenation) model and a rat myocardial I/R injury model.
View Article and Find Full Text PDFDownregulation of fibroblast growth factor 5 inhibits cell growth and invasion of human nonsmall-cell lung cancer cells.
J Cell Biochem
May 2019
Department of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou, China.
The morbidity and mortality rates of nonsmall-cell lung cancer (NSCLC) have increased in recent years. We aimed to explore the biological role of fibroblast growth factor 5 (FGF5) in NSCLC. We first established that the expression of FGF5 was increased in NSCLC tissues compared with the normal adjacent tissues.
View Article and Find Full Text PDFMicroRNA-98-5p inhibits proliferation and metastasis in non-small cell lung cancer by targeting TGFBR1.
Int J Oncol
January 2019
Department of Cardiothoracic Surgery, Wujin People's Hospital of Changzhou, Changzhou, Jiangsu 213017, P.R. China.
MicroRNAs (miRNAs or miRs) have recently emerged as key regulators of various types of cancer, including non‑small cell lung cancer (NSCLC). The disrupted expression of miRNAs is associated with tumorigenesis and metastasis; however, the underlying mechanisms remain unclear. In this study, we demonstrate that miR‑98‑5p is downregulated in NSCLC and that miR‑98‑5p deficiency is associated with an advanced clinical stage and metastasis.
View Article and Find Full Text PDFBlockage of AKAP12 accelerates angiotensin II (Ang II)-induced cardiac injury in mice by regulating the transforming growth factor β1 (TGF-β1) pathway.
Biochem Biophys Res Commun
May 2018
Department of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China. Electronic address:
Article Synopsis
- Hypertension causes cardiac remodeling and is linked to a protein called A-kinase anchor protein 12 (AKAP12), which helps regulate blood vessel integrity, but its role in cardiac injury from angiotensin II (Ang II) is not well understood.
- The study found that Ang II infusion lowered AKAP12 levels in wild-type mice, while AKAP12 knockout led to increased inflammation, quicker heart damage, and worsened heart failure symptoms.
- Results indicate that AKAP12 helps protect against fibrosis induced by Ang II, possibly by inactivating the TGF-β1 pathway, as evidenced by various molecular analyses showing increased fibrosis markers in AKAP12-deficient mice.