缺氧誘導因子與廣鹽性硬骨魚類滲透壓生理調節之關聯

Abstract

穩定體液滲透度是廣鹽性魚類在遭遇環境鹽度變異時重要的生理適應策略。而眾多非生物性環境擾動均會影響生物缺氧誘導因子(HIFs)蛋白功能的穩定性，進而影響細胞運作。然而目前對於魚類面臨滲透壓波動挑戰時，細胞內HIFs相關訊息網絡與滲透壓恆定的研究仍非常缺乏。本研究選用India medaka (Oryzias melastigma)作為暴露高鹽環境的廣鹽性硬骨魚實驗物種，實驗結果發現其仔魚在面臨鹽度上升刺激時，HIF-1α的基因和蛋白質表現量皆會顯著上升，而部分HIF-1α的核酸訊號亦會表現在仔魚表皮的離子細胞。此外，HIF-1α蛋白的弱化處理，除了會顯著地影響仔魚鈉鉀幫浦的蛋白表現量，亦會降低其在高鹽處理時表皮對於鈉與氯離子的排放；然而，仔魚表皮上離子細胞的表現密度，並未受到HIF-1α蛋白的弱化影響。我們據此推論：HIF-1α於表皮細胞的表現，有助於廣鹽性魚類在面臨環境鹽度挑戰時進行體液調節機制。Maintenance of osmostasis is one of the most important physiological processes for euryhaline teleosts to cope with ambient salinity challenges. And hypoxia-inducible factors (HIFs) were found to be involved in several cellular regular functions under diverse abiotic perturbations. However, HIFs-related signaling for osmostasis in euryhaline teleosts under osmotic challenges are still unknown. In this study, India medaka (Oryzias melastigma) was utilized as an euryhaline teleost model to study the possible roles of HIFs for hyperosmotic adaptation. Based on eveluations of transcripts and protein expressions, ambient salinity challenges apparently up-regulated HIF-1 expressions in madaka larvae, and HIF-1 homologue (hif-1al) was partially expressed in Na+/K+-ATPase (NKA)-positive epithelial cells. Moreover, abrogation of HIF-1α-like obviously depressed NKA protein expression as well as sodium and chloride effluxes from yolk sac epithelium in seawater condition, while NKA-positive cell density on epithelium was not changed in HIF-1α-like morphants in comparison to mismatch control ones. Consequently, HIF-1α expression and stabilization in epithelium are essential for maintaining osmostasis in euryhaline teleosts under salinity challenges.