Anti-SOD2 (full length) polyclonal antibody [Biotin]

Recently, there has been increased studies in noise-induced hearing loss (NIHL). We aimed to make an overview of research trends and genetic polymorphisms for NIHL from 2009 to 2018 with VOSviewer software. A total of 2391 papers were identified for research trends analysis in NIHL and 33 studies identified for a brief review of genetic polymorphisms in human NIHL. The number of publications has been increasing over the past decade. The journal Hearing Research published the most articles (218). The USA contributed the largest number of papers (1042; 43.58%), with the most citations (18,987) and the highest H-index (60). The University of Washington was the most contributive institution. Liberman MC published the most articles (32), and Kujawa SG possessed the highest co-citations (584). Except for high-frequency keywords identified by the software, "prevalence," "oxidative stress," "hair cells," and "cochlear implant" were also the latest research frontiers. HSPA1A rs1043618, HSPA1L rs2227956, PON2 rs12026 and rs7785846, SOD2 rs2855116, KCNE1 rs2070358, KCNQ4 rs34287852, GJB2 rs3751385, PCDH15 rs7095441 and rs11004085, GRHL2 rs1981361, ITGA8 rs10508489, MYH14 rs667907, and POU4F3 rs891969 were the research hotspots and were replicated in independent samples. Inflammation response underlying NIHL has emerged and should be considered as a pioneering field in the future for the prevention of NIHL and conservation of hearing.

Persistent pulmonary hypertension of the newborn (PPHN) is a failure of pulmonary vascular resistance to decline at birth rapidly. One principal mechanism implicated in PPHN development is mitochondrial oxidative stress. Expression and activity of mitochondrial SOD2 (superoxide dismutase) are decreased in PPHN; however, the mechanism remains unknown. Recently, OLA1 (Obg-like ATPase-1) was shown to act as a critical regulator of proteins controlling cell response to stress including Hsp70, an obligate chaperone for SOD2. Here, we investigated whether OLA1 is causally linked to PPHN. Compared with controls, SOD2 expression is reduced in distal-pulmonary arteries (PAs) from patients with PPHN and fetal-lamb models. Disruptions of the SOD2 gene reproduced PPHN phenotypes, manifested by elevated right ventricular systolic pressure, PA-endothelial cells apoptosis, and PA-smooth muscle cells proliferation. Analyses of SOD2 protein dynamics revealed higher ubiquitinated-SOD2 protein levels in PPHN-lambs, suggesting dysregulated protein ubiquitination. OLA1 controls multiple proteostatic mechanisms and is overexpressed in response to stress. We demonstrated that OLA1 acts as a molecular chaperone, and its activity is induced by stress. Strikingly, OLA1 expression is decreased in distal-PAs from PPHN-patients and fetal-lambs. OLA1 deficiency enhanced CHIP affinity for Hsp70-SOD2 complexes, facilitating SOD2 degradation. Consequently, mitochondrial H2O2 formation is impaired, leading to XIAP (X-linked inhibitor of apoptosis) overexpression that suppresses caspase activity in PA-smooth muscle cells, allowing them to survive and proliferate, contributing to PA remodeling. In-vivo, ola1(-/-) downregulated SOD2 expression, induced distal-PA remodeling, and right ventricular hypertrophy. We conclude that decreased OLA1 expression accounts for SOD2 downregulation and, therefore, a therapeutic target in PPHN treatments.