A subfraction obtained from the venom of the tarantula Poecilotheria regalis contains inhibitor cystine knot peptides and induces relaxation of rat aorta by inhibiting L-type voltage-gated calcium channels

IF 3.6 Q2 TOXICOLOGY Toxicon: X Pub Date : 2023-06-01 DOI:10.1016/j.toxcx.2023.100151
Luis Fernando Díaz-Peña , Torres-Ortiz Daniela , Manuel B. Aguilar , Enoch Luis , Fernando Lazcano-Pérez , Roberto Arreguín-Espinosa , Arturo Hernandez-Cruz , César Ibarra-Alvarado , Alejandro García-Arredondo
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引用次数: 1

Abstract

Venoms from tarantulas contain low molecular weight vasodilatory compounds whose biological action is conceived as part of the envenomation strategy due to its propagative effects. However, some properties of venom-induced vasodilation do not match those described by such compounds, suggesting that other toxins may cooperate with these ones to produce the observed biological effect. Owing to the distribution and function of voltage-gated ion channels in blood vessels, disulfide-rich peptides isolated from venoms of tarantulas could be conceived into potential vasodilatory compounds. However, only two peptides isolated from spider venoms have been investigated so far. This study describes for the first time a subfraction containing inhibitor cystine knot peptides, PrFr-I, obtained from the venom of the tarantula Poecilotheria regalis. This subfraction induced sustained vasodilation in rat aortic rings independent of vascular endothelium and endothelial ion channels. Furthermore, PrFr-I decreased calcium-induced contraction of rat aortic segments and reduced extracellular calcium influx to chromaffin cells by the blockade of L-type voltage-gated calcium channels. This mechanism was unrelated to the activation of potassium channels from vascular smooth muscle, since vasodilation was not affected in the presence of TEA, and PrFr-I did not modify the conductance of the voltage-gated potassium channel Kv10.1. This work proposes a new envenomating function of peptides from venoms of tarantulas, and establishes a new mechanism for venom-induced vasodilation.

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从狼蛛毒液中获得的一个亚组分含有抑制剂胱氨酸结肽,并通过抑制L型电压门控钙通道诱导大鼠主动脉舒张
狼蛛的毒液含有低分子量的血管舒张化合物,由于其繁殖作用,其生物作用被认为是环境形成策略的一部分。然而,毒液诱导的血管舒张的一些特性与这些化合物所描述的特性不匹配,这表明其他毒素可能与这些毒素合作产生观察到的生物效应。由于电压门控离子通道在血管中的分布和功能,从狼蛛毒液中分离出的富含二硫化物的肽可以被认为是潜在的血管舒张化合物。然而,到目前为止,只有两种从蜘蛛毒液中分离的肽被研究过。本研究首次描述了从狼蛛毒液中获得的含有抑制剂胱氨酸结肽PrFr-I的亚组分。该亚组分在不依赖于血管内皮和内皮离子通道的大鼠主动脉环中诱导持续的血管舒张。此外,PrFr-I通过阻断L型电压门控钙通道,减少了钙诱导的大鼠主动脉段收缩,并减少了细胞外钙流入嗜铬细胞。该机制与血管平滑肌钾通道的激活无关,因为在TEA存在的情况下血管舒张不受影响,并且PrFr-I不会改变电压门控钾通道Kv10.1的电导。这项工作提出了狼蛛毒液肽的一种新的环境交配功能,并建立了毒液诱导血管舒张的新机制。
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来源期刊
Toxicon: X
Toxicon: X Pharmacology, Toxicology and Pharmaceutics-Toxicology
CiteScore
6.50
自引率
0.00%
发文量
33
审稿时长
14 weeks
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