Comparative Transcriptomic Analysis to Identify the Important Coding and Non-coding RNAs Involved in the Pathogenesis of Pterygium.

Pterygium is a common ocular surface disease characterized by abnormal fibrovascular proliferation and invasion, similar to tumorigenesis. The formation of tumors is related to a change in the expression of various RNAs; however, whether they are involved in the formation and development of pterygium remains unclear. In this study, transcriptome analysis of messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) of paired pterygium and normal conjunctiva was performed to explore key genes regulating the development of pterygium.

Transcriptome-wide study of the response of human trabecular meshwork cells to the substrate stiffness increase.

Elevated intraocular pressure, a major risk factor of glaucoma, is caused by the abnormal function of trabecular outflow pathways. Human trabecular meshwork (HTM) tissue plays an important role in the outflow pathways. However, the molecular mechanisms that how TM cells respond to the elevated IOP are largely unknown.

AFC1 Compound Attenuated MI/R-Induced Ventricular Remodeling Inhibiting PDGFR and STAT Pathway.

Effective interventions to improve the outcome of patients subjected to myocardial ischemia reperfusion (MI/R) are urgent in clinical settings. Tanshinone IIA (TSA) is reported to attenuate myocardial injury and improve ventricular remodeling post MI/R. Here, we evaluated the efficacy of AFC1 compound that is similar to TSA structure in murine MI/R models.

Dynamic Profile of CD4 T-Cell-Associated Cytokines/Chemokines following Murine Myocardial Infarction/Reperfusion.

CD4 T-cells play crucial roles in the injured heart. However, the way in which different CD4 T subtypes function in the myocardial infarction/reperfusion (MI/R) heart is still poorly understood. We aimed to detect the dynamic profile of distinct CD4 subpopulation-associated cytokines/chemokines by relying on a closed-chest acute murine MI/R model.

IL-17 contributes to the pathogenesis of obliterative bronchiolitis via regulation of M1 macrophages polarization in murine heterotopic trachea transplantation models.

Acute allograft rejection is a principal conundrum in lung obliterative bronchiolitis (OB). Monocytes/macrophages infiltration has been proved to be the main reason for acute rejection. IL-17 contributes to the recruitment and function of macrophages.