Brain Regulatory Mechanism Microvascular

Brain Regulatory Mechanism

The vascular system of the SNC comes from the embryonic development by angiogenesis as blood vessels on the leptotene surface develop towards the parenchyma (Marin-Padilla, 1985), and, in this way, the CNS vessels and the microvasculature are exclusively formed by angiogenic processes of the vascular plexus per inmate (flame et al., 1997). 

Angiogenesis implies the creation of new blood vessels by germinating or diverging pre-existing vessels, giving birth to the SNC micro vascularization network. Cellular and molecular mechanisms are involved in maintaining an appropriate cerebral microvasculature, in which cellular scaffolding and molecular exchange are intimately linked. 

In addition, epigenetics, gene switching, cytokines, and extracellular matrix molecules (ECM) are also involved in maintaining the good performance of the neurovascular unit, not only in physiological conditions but also under pathological stimuli.

Cellular mechanisms

The physical and biological characteristics of cerebral vascularization are supplied by endothelial cells (EC), pericytes, smooth muscle cells also known as wall cells, or red mullet cells, and astroglial foot processes (Giannoni et al.,, 2018; Sweeney et al., 2019), which, with neurons, constitute the neurovascular unit (Iadecola, 2017; McConnell et al., 2017) (fig. 

  • This concept of a neurovascular unit emerged in 2001, at the meeting of the Actual Examination Group of the National Institute of Neurological Disorders and Cerebral Vascular Accidents (HTTPS: //www.nia.NIH. Gov / Health / Vascular-Contribution-Cognitive-Impairment and-Dementia) to strengthen the close connection between a correct CNS function and its micro vascularization, obtained by effective paracrine regulations
  • Signals and interactions of the extracellular matrix. ECM is essential to provide signals to achieve the survival of adequate vascular cells, proliferation, migration, differentiation, and maturation to establish a functional vascular network where the emerging vessels were matured into sustainable, stable vessels, not light and functional. 

During maturation, the new ship is surrounded by pericytes, which inhibit the proliferation of CE (Folkman and Amore, 1996), but if the stabilization of the vessels does not occur, then the immature ship undergoes apoptosis (youngest and al., 1998). It is proven that ECM-Integrin interactions play an important role in regulating vessel maturation in the SNC (Milner and Campbell, 2002). 

In this sense, it has been demonstrated in development mice that the maturation of the SNC blood vessel was accompanied by an increased expression of integrin B1 as well as A4 and A5 integrins in early development, and with A1 and A6 in late development and adulthood (Milner (Milner and Campbell, 2002). 

In pathophysiological conditions, AVB3 integrins are expressed in activated micro visseaux of SNC and have essential functions in the activation of angiogenesis which occurs in cerebral ischemia (Abumiya et al., 1999). In the opposite scenario, antagonism of the AV integrin was used in experimental models to reduce the size of the cerebral glioma by inhibiting angiogenesis (Macdonald et al., 2001).

  • MicroRNAs.  Interestingly, the vascularization of the SNC is also regulated epigenetically by micro yarn (Mirs). These small non-coding RNA molecules from 22 to 24 nucleotides in length play a relevant role in a wide variety of biological processes through the post-transcriptional modulation of genes. 

Recent studies have indicated the key function of the Mirs in the regulation of angiogenesis (SURSERE and SESSSA, 2009) (Fig. 3). Some of them, in particular the Mir-9 and Mir-30 families, are mainly involved in the development of the SNC vascular system (Cho et al., 2019; Madelaine et al., 2017).

Source

Gallego, I., Villate-Beitia, I., Saenz-del-Burgo, L., Puras, G., & Pedraz, J. L. (2022). Therapeutic Opportunities and Delivery Strategies for Brain Revascularization in Stroke, Neurodegeneration, and Aging. Pharmacological Reviews74(2), 439-461.

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