Protective mechanism of fdft1 in steroid hormone synthesis pathway in SD rats with acute hypoxic injury
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Online ISSN 2092-9293 Print ISSN 1976-9571
RESEARCH ARTICLE
Protective mechanism of fdft1 in steroid hormone synthesis pathway in SD rats with acute hypoxic injury Xue Lin1 · Haiyan Wang1 · Xiaoyan Pu1,2 Received: 26 May 2020 / Accepted: 11 September 2020 © The Genetics Society of Korea 2020
Abstract Background The acute hypoxic injury caused by the plain population entering the plateau in a short period of time has become the main cause of endangering the health of the people who rush into the plateau. Objective The study aimed to identify the key genes which participate in resisting the acute hypoxic injury in SD Rats by transcriptomic profile analysis. Methods 48 Sprague Dawley (SD) male rats were enrolled and randomly divided into four groups (0h, 24h, 48h, 72h) and housed in hypobaric hypoxia chamber with altitude 6000m for different periods of time to make them acute hypoxic injury. The transcriptomic profile of the lung tissue of the rats was analysed by RNA second-generation sequencing combined with bioinformatics analysis. Results The results of GO and KEGG function classification analysis revealed that the differential expression genes enriched in steroid hormone synthesis pathway especially in 48h group compared to F0 group. Further analysis revealed that Farnesyl Diphosphate Farnesyl Transferase 1 (fdft1) gene encoding a rate-limiting enzyme in steroid hormone synthesis pathway was significant differently expressed between the groups. The expression levels of fdft1 gene were further verified by RT-PCR and Western-blot methods. Conclusions The results suggest that fdft1 gene plays an important role in responding to acute hypoxic injury by regulating steroid hormone biosynthesis. Keywords Hypoxia · Acute hypoxic injury · Transcriptomic analysis · fdft1 gene · 1,25 Dihydroxyvitamin D3
Introduction High altitude hypoxia can induce complex inflammatory response and led to acute hypoxic injury to the lung of the individuals who ascends to high altitudes (above 2500–3000 m) rapidly (Hanaoka et al. 2000; Mishra et al. 2016; Basnyat and Murdoch 2003; Agorreta and Zulueta 2005). Hypobaric hypoxia can induce accumulation of erythrocytes in lung due to the breakdown of alveolar capillary Electronic supplementary material The online version of this article (https://doi.org/10.1007/s13258-020-00999-5) contains supplementary material, which is available to authorized users. * Xiaoyan Pu [email protected] 1
College of Medicine, Qinghai University, Xining, Qinghai, China
Qinghai Normal University, Xining, Qinghai, China
2
barrier and cause high pulmonary-artery pressure (Agorreta et al. 2003; Brtsch 2015). If not treated timely and properly, acute hypoxic injury may develop into life-threatening high altitude pulmonary edema (HAPE) (Yarnell et al. 2000; Sartori et al. 2002; Stream and Grissom 2008; Voelkel 2002). HAPE is an acute high altitude disease which is characterized by pulmonary interstitial or alveolar edema due to acute hypoxia and is the main cause of death of high altitude disease. St
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