類雌激素受體在日本稻田魚表皮排酸功能調控之角色

Abstract

魚類面臨環境酸化壓力時，體內的血液滲透壓及pH值隨之下降，需大量耗能以恢復體內離子及酸鹼恆定。隨著工業發展，環境污染及氣候變遷造成全球水域的酸化，使魚類生存受到了壓迫，因此，了解魚類酸鹼調節機制是極為重要的課題。神經內分泌系統是生物連結外在環境的重要橋樑，生物遭遇逆境時賀爾蒙將會進行調控，以達最適生存的狀態。Estrogen-related receptors (ERRs) 是孤兒細胞核受體，在生物面臨壓力或刺激時，會參與回應環境適應，已知ERRs在哺乳類會影響Na+、K+的調節，在斑馬魚(Denio rerio)會參與排除H+。斑馬魚主要是由離子細胞上的H+-ATPase (HA)進行排酸，但日本稻田魚、吳郭魚(Oreochromis mossambica)等大多數淡水魚卻主要是以Na+/H+ exchanger 3 (NHE3)進行排酸。因此在本研究中以日本稻田魚作為模式生物探討ERRs對於其離子調控所扮演的角色。在本文發現，日本稻田魚受酸刺激後，其體內及鰓上的errγ2基因表現量有顯著上升。在抑制ERRα以及ERRγ2兩型受體蛋白的實驗中，發現α型不藉由影響離子細胞的數目而直接影響NHE3的表現量進而參與排酸機制；另一方面，結果也顯示，α與γ2型可能也會經由其他途徑間接參與日本稻田魚的排酸機制。此外，螢光原位雜合與免疫螢光染色的結果也支持了前述的假設。但ERRs作用在日本稻田魚的機制仍不明確，有待繼續研究探討。

When fish are encountering an acidic stress, they have to consume extra energy to restore the disturbed internal ionic and acid-base homeostasis. Following the development of industry, environmental pollution and climate change cause acidification in global water and have been threatening the survival of fish. Therefore, studying acid-base regulation mechanisms in fish is extremely important to understand how fish cope with environmental acidification. While fish face a tension, the role of neuroendocrine system is a link between physiological responses and environmental changes. When under stress, estrogen-related receptors (ERRs), steroid hormone receptors, contribute to adapt environment in organisms. In a previous study, ERRs was found to affect V-type H+-ATPase (HA), the major proton secretion related transporter, to regulate proton secretion in zebrafish (Denio rerio). Most of freshwater fishes, such as medaka (Oryzias latipes) and tilapia (Oreochromis mossambicus), use Na+/H+ exchanger 3 (NHE3) as the major proton secretion transporter. Therefore, the present study used medaka as the model animal to investigate the role of ERRs in regulation of proton secretion. Under acidic stress, errγ2 mRNA expression of embryos and adult gills were upregulated. ERRα or ERRγ2 knockdown experiments revealed that ERRα may enhance the expression of NHE3 rather than affecting differentiation of ionocytes to directly regulate H+secretion. The results also suggested that ERRα and ERRγ2 may indirectly affect acid secretion function via other pathways to regulate the function of ionocytes to achieve body fluid acid-base homeostasis; however, the detailed mechanisms are needed to be clarified in future studies.