Publications by authors named "Muhammad Abdul Rouf"

2 Publications

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The blood flow-klf6a-tagln2 axis drives vessel pruning in zebrafish by regulating endothelial cell rearrangement and actin cytoskeleton dynamics.

PLoS Genet 2021 Jul 28;17(7):e1009690. Epub 2021 Jul 28.

Key Laboratory for Biorheological Science and Technology of Ministry of Education, Bioengineering College of Chongqing University, Chongqing, China.

Recent studies have focused on capillary pruning in various organs and species. However, the way in which large-diameter vessels are pruned remains unclear. Here we show that pruning of the zebrafish caudal vein (CV) from ventral capillaries of the CV plexus in different transgenic embryos is driven by endothelial cell (EC) rearrangement, which involves EC nucleus migration, junction remodeling, and actin cytoskeleton remodeling. Further observation reveals a growing difference in blood flow velocity between the two vessels in CV pruning in zebrafish embryos. With this model, we identify the critical role of Kruppel-like factor 6a (klf6a) in CV pruning. Disruption of klf6a functioning impairs CV pruning in zebrafish. klf6a is required for EC nucleus migration, junction remodeling, and actin cytoskeleton dynamics in zebrafish embryos. Moreover, actin-related protein transgelin 2 (tagln2) is a direct downstream target of klf6a in CV pruning in zebrafish embryos. Together these results demonstrate that the klf6a-tagln2 axis regulates CV pruning by promoting EC rearrangement.
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http://dx.doi.org/10.1371/journal.pgen.1009690DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8318303PMC
July 2021

Progress and prospects of mechanotransducers in shear stress-sensitive signaling pathways in association with arteriovenous malformation.

Clin Biomech (Bristol, Avon) 2021 Jun 24;88:105417. Epub 2021 Jun 24.

Key Laboratory for Biorheological Science and Technology of Ministry of Education State and Local Joint Engineering Laboratory for Vascular Implants Bioengineering College of Chongqing University, Chongqing 400030, China. Electronic address:

Arteriovenous malformations are congenital vascular lesions characterized by a direct and tangled connection between arteries and veins, which disrupts oxygen circulation and normal blood flow. Arteriovenous malformations often occur in the patient with hereditary hemorrhagic telangiectasia. The attempts to elucidate the causative factors and pathogenic mechanisms of arteriovenous malformations are now still in progress. Some studies reported that shear stress in blood flow is one of the factors involved in arteriovenous malformations manifestation. Through several mechanotransducers harboring the endothelial cells membrane, the signal from shear stress is transduced towards the responsible signaling pathways in endothelial cells to maintain cell homeostasis. Any disruption in this well-established communication will give rise to abnormal endothelial cells differentiation and specification, which will later promote arteriovenous malformations. In this review, we discuss the update of several mechanotransducers that have essential roles in shear stress-induced signaling pathways, such as activin receptor-like kinase 1, Endoglin, Notch, vascular endothelial growth factor receptor 2, Caveolin-1, Connexin37, and Connexin40. Any disruption of these signaling potentially causes arteriovenous malformations. We also present some recent insights into the fundamental analysis, which attempts to determine potential and alternative solutions to battle arteriovenous malformations, especially in a less invasive and risky way, such as gene treatments.
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http://dx.doi.org/10.1016/j.clinbiomech.2021.105417DOI Listing
June 2021
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