Department of Physiology, Wayne State University School of Medicine, Detroit, MI, United States.
Vitam Horm. 2020;112:147-162. doi: 10.1016/bs.vh.2019.08.007. Epub 2019 Oct 18.
Secretory vesicle swelling has been demonstrated to be a requirement in cell secretion. In the past 25 years, the quest to elucidate the molecular mechanism of secretory vesicle swelling, serendipitously revealed the presence of water channels or aquaporins at the secretory vesicle membrane and their involvement in rapid gaiting of water into secretory vesicles and their swelling during secretion. These studies further provided an understanding of aquaporin regulation at the secretory vesicle membrane. Secretory vesicles within live cells, isolated secretory vesicles, single vesicle electrophysiological patch clamp studies and the swelling complex reconstituted into liposomes, have all been utilized to elucidate the mechanism and regulation of secretory vesicle swelling. Results from these studies collectively demonstrate the involvement of β-adrenergic receptor, heterotrimeric GTP-binding G-proteins such as GαI; PLA2 and potassium and chloride channels, in the regulation of aquaporins at the secretory vesicle membrane.
已证实分泌小泡肿胀是细胞分泌的必要条件。在过去的 25 年中，人们一直在探索阐明分泌小泡肿胀的分子机制，偶然发现水通道或水通道蛋白存在于分泌小泡膜上，并且它们参与了水向分泌小泡的快速运动以及分泌过程中小泡的肿胀。这些研究进一步了解了分泌小泡膜上水通道蛋白的调节。利用活细胞内的分泌小泡、分离的分泌小泡、单个小泡电生理膜片钳研究以及重新构成脂质体的肿胀复合物，阐明了分泌小泡肿胀的机制和调节。这些研究的结果共同表明，β-肾上腺素能受体、异三聚体 GTP 结合 G 蛋白（如 GαI）、PLA2 和钾、氯离子通道参与了分泌小泡膜上水通道蛋白的调节。
