Development of the renal vasculature

Mohamed, Tahagod; Sequeira-Lόpez, Maria Luisa S.

doi:10.1016/j.semcdb.2018.06.001

Cited by 40 publications

(35 citation statements)

References 175 publications

(233 reference statements)

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“…They concluded that LYVE-1 + cells initially bud off from veins but that LYVE-1 + macrophages and dendritic cells are crucial in orchestrating a branching process that connects these cells to extra-renal lymphatic vessels. VEGF-C also seems to have an essential regulatory role in this branching process ( Lee et al, 2011 ; Mohamed and Sequeira-Lopez, 2018 ). Tanabe et al (2012) similarly found that renal lymphatic vessels in the rat develop initially from pre-existing extrarenal lymphatic vessels and extend toward the cortex along the renal blood vasculature.…”

Section: Anatomy Of Renal Lymphaticsmentioning

confidence: 99%

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

et al. 2019

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Renal lymphatics are abundant in the cortex of the normal kidney but have been largely neglected in discussions around renal diseases. They originate in the substance of the renal lobule as blind-ended initial capillaries, and can either follow the main arteries and veins toward the hilum, or penetrate the capsule to join capsular lymphatics. There are no valves present in interlobular lymphatics, which allows lymph formed in the cortex to exit the kidney in either direction. There are very few lymphatics present in the medulla. Lymph is formed from interstitial fluid in the cortex, and is largely composed of capillary filtrate, but also contains fluid reabsorbed from the tubules. The two main factors that contribute to renal lymph formation are interstitial fluid volume and intra-renal venous pressure. Renal lymphatic dysfunction, defined as a failure of renal lymphatics to adequately drain interstitial fluid, can occur by several mechanisms. Renal lymphatic inflow may be overwhelmed in the setting of raised venous pressure (e.g., cardiac failure) or increased capillary permeability (e.g., systemic inflammatory response syndrome). Similarly, renal lymphatic outflow, at the level of the terminal thoracic duct, may be impaired by raised central venous pressures. Renal lymphatic dysfunction, from any cause, results in renal interstitial edema. Beyond a certain point of edema, intra-renal collecting lymphatics may collapse, further impairing lymphatic drainage. Additionally, in an edematous, tense kidney, lymphatic vessels exiting the kidney via the capsule may become blocked at the exit point. The reciprocal negative influences between renal lymphatic dysfunction and renal interstitial edema are expected to decrease renal function due to pressure changes within the encapsulated kidney, and this mechanism may be important in several common renal conditions.

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Section: Anatomy Of Renal Lymphaticsmentioning

confidence: 99%

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

et al. 2019

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“…The issue of the development of the kidney vascularization is highly controversial [32]. Compelling evidence of sprouting angiogenesis has been provided [33].…”

Section: Discussionmentioning

confidence: 99%

Contribution of a GATA4-Expressing Hematopoietic Progenitor Lineage to the Adult Mouse Endothelium

Carmona

Moral

Barrena

et al. 2020

Cells

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Different sources have been claimed for the embryonic origin of the coronary endothelium. Recently, the potential of circulating cells as progenitors of the cardiac endothelium has also been suggested. In a previous study we have shown that circulating progenitors are recruited by the embryonic endocardium and incorporated into the coronary vessels. These progenitors derive from a mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2. Herein, we aim to trace this specific lineage throughout postnatal stages. We have found that more than 50% of the adult cardiac endothelium derives from the G2-GATA4 lineage. This percentage increases from embryos to adults probably due to differential proliferation and postnatal recruitment of circulating endothelial progenitors. In fact, injection of fetal liver or placental cells in the blood stream of neonates leads to incorporation of G2-GATA4 lineage cells to the coronary endothelium. On the other hand, labeling of the hematopoietic lineage by the stage E7.5 also resulted in positive coronary endothelial cells from both, embryos and adults. Our results suggest that early hematopoietic progenitors recruited by the embryonic ventricular endocardium can become the predominant source of definitive endothelium during the vascularization of the heart.

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“…Angiogenesis is the formation of new blood vessels from the preexisting capillary network, which is a vital process in normal tissue development as well as the progression of several diseases, including inflammation, cancer, and diabetes (Musa et al, ; Mohamed and Sequeira‐Lopez, ). In the central nervous system, cerebral angiogenesis plays a role not only in the formation of brain vasculature during development but also in pathological events, such as the recovery of circulation after an ischemic stroke (Ruan et al, ).…”

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confidence: 99%

Atg7 Silencing Inhibits Laminin‐5 Expression to Suppress Tube Formation by Brain Endothelial Cells

Wei

Liu

et al. 2019

The Anatomical Record

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Cerebral angiogenesis is a key event during brain development and recovery from brain injury. We previously demonstrated that Atg7 knockout impaired angiogenesis in the mouse brain. However, the role of Atg7 in angiogenesis is not completely understood. In this study, we used human brain microvascular endothelial cells (HBMECs) to investigate the mechanism of Atg7‐regulated cerebral angiogenesis. We found that Atg7 depletion specifically diminished the expression of the β3 and γ2 chains of laminin‐5, a major component of the extracellular matrix. In contrast, autophagy inhibitors did not affect laminin‐5 expression, suggesting that Atg7‐regulated laminin‐5 expression is autophagy‐independent. We also found that Atg7‐regulated laminin‐5 expression occurred at the transcriptional level through NF‐κB signaling. Exogenous laminin‐5 or the NF‐κB agonist betulinic acid effectively rescued tube formation by Atg7‐deficient HBMECs. Taken together, our study identified a novel mechanism by which Atg7 regulates laminin‐5 expression via NF‐κB to modulate tube formation by brain endothelial cells during cerebral angiogenesis. Anat Rec, 302:2255–2260, 2019. © 2019 American Association for Anatomy

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Development of the renal vasculature

Cited by 40 publications

References 175 publications

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

Contribution of a GATA4-Expressing Hematopoietic Progenitor Lineage to the Adult Mouse Endothelium

Atg7 Silencing Inhibits Laminin‐5 Expression to Suppress Tube Formation by Brain Endothelial Cells

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