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小分子 GTP 酶 Rif 在小鼠血小板丝状伪足的生成中不是必需的。

The small GTPase Rif is dispensable for platelet filopodia generation in mice.

机构信息

School of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom.

出版信息

PLoS One. 2013;8(1):e54663. doi: 10.1371/journal.pone.0054663. Epub 2013 Jan 24.

DOI:10.1371/journal.pone.0054663
PMID:23359340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3554654/
Abstract

BACKGROUND

Formation of filopodia and other shape change events are vital for platelet hemostatic function. The mechanisms regulating filopodia formation by platelets are incompletely understood however. In particular the small GTPase responsible for initiating filopodia formation by platelets remains elusive. The canonical pathway involving Cdc42 is not essential for filopodia formation in mouse platelets. The small GTPase Rif (RhoF) provides an alternative route to filopodia generation in other cell types and is expressed in both human and mouse platelets.

HYPOTHESIS/OBJECTIVE: We hypothesized that Rif might be responsible for generating filopodia by platelets and generated a novel knockout mouse model to investigate the functional role of Rif in platelets.

METHODOLOGY/PRINCIPAL FINDINGS: Constitutive RhoF(-/-) mice are viable and have normal platelet, leukocyte and erythrocyte counts and indices. RhoF(-/-) platelets form filopodia and spread normally on various agonist surfaces in static conditions and under arterial shear. In addition, RhoF(-/-) platelets have normal actin dynamics, are able to activate and aggregate normally and secrete from alpha and dense granules in response to collagen related peptide and thrombin stimulation.

CONCLUSIONS

The small GTPase Rif does not appear to be critical for platelet function in mice. Functional overlap between Rif and other small GTPases may be responsible for the non-essential role of Rif in platelets.

摘要

背景

血小板止血功能的形成需要伪足和其他形状变化事件。然而，调节血小板伪足形成的机制尚未完全了解。特别是负责启动血小板伪足形成的小 GTPase 仍然难以捉摸。涉及 Cdc42 的经典途径对于小鼠血小板伪足的形成不是必需的。小 GTPase Rif（RhoF）为其他细胞类型的伪足生成提供了另一种途径，在人和小鼠血小板中均有表达。

假设/目的：我们假设 Rif 可能负责生成血小板伪足，并生成了一种新型的敲除小鼠模型来研究 Rif 在血小板中的功能作用。

方法/主要发现：组成型 RhoF(-/-) 小鼠具有活力，并且血小板、白细胞和红细胞计数和指数正常。RhoF(-/-) 血小板在静态条件下和动脉剪切下在各种激动剂表面上形成伪足并正常扩散。此外，RhoF(-/-) 血小板具有正常的肌动蛋白动力学，能够正常激活和聚集，并在胶原相关肽和凝血酶刺激下从α和致密颗粒中分泌。

结论

小 GTPase Rif 似乎对小鼠血小板功能不是必需的。Rif 和其他小 GTPase 之间的功能重叠可能是 Rif 在血小板中非必需作用的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/0233e39cead6/pone.0054663.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/e938b3208213/pone.0054663.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/eed10f2c0417/pone.0054663.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/0233e39cead6/pone.0054663.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/e938b3208213/pone.0054663.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/eed10f2c0417/pone.0054663.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd08/3554654/0233e39cead6/pone.0054663.g003.jpg

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