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Craniofacial Regeneration—Bone
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Laura Guadalupe Hernandez, Lucia Pérez Sánchez, Rafael Hernández González, Janeth Serrano-Bello
Blood vessels of the bone develop through the process of angiogenesis, which involves the proliferation of local endothelial cells to produce new blood vessels from pre-existing vessels in a remodeling process. The vasculogenesis is the formation of a vascular network, from a progenitor cell, angioblast or hemangioblast. The blood vessels supply the bone system with nutrients and oxygen, excrete waste biological materials, remove metabolites from the bone, provide the bone with specific hormones, growth factors and neurotransmitters secreted by other tissues, maintaining the bone cells survival and stimulating their activity. The craniofacial bones develop by two processes: intramembranous ossification and endochondral ossification. Intramembranous ossification is the main mechanism leading to a development of flats bones (e.g., maxillae, palatal bones, nasal bones, zygomatic bones) this process is related to a direct differentiation of mesenchymal stem cells into osteoblasts, initially with a fibrous membrane and finally replaced by a spongy bone, whereas the endochondral ossification is typical of long bones and the cranial base, this process has an intermediate stage with cartilage (Chu et al. 2014; Fishero et al. 2014; Filipowska et al. 2017). The development and maintenance of the endochondral and intramembranous bone formation are dependent on the bone vascular network (Filipowska et al. 2017; Prisby 2017).
Oxidative stress and pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
Vascular endothelial growth factors (VEGFs) are a subfamily of growth factors derived from platelets or platelet-derived growth factors. They are known to be decreased in pre-eclampsia.38 VEGF production and behaviour seems to have an interesting role in the causation pathology of pre-eclampsia. The VEGF are a signal protein produced by cells at different locations of the body. Their essential role is to stimulate formation of new vessels and maintain these vessels functionally and structurally (vasculogenesis and angiogenesis). Vasculogenesis involves de novo formation of embryonic circulatory systems, and angiogenesis means growth and renovation of already existing vascular system. They have a role in health as well as in disease. The VEGF have a big role in supporting embryonic development.39 They are believed to have a critical role in the aetiology of endometriosis.40
Biological basis of angiogenesis and role of vascular endothelial growth factor-D
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
Blood vessel development is an essential requirement for development of the embryo as well as for adult functions such as reproduction and wound healing. Vasculogenesis refers to the differentiation of vascular precursors to endothelial cells assembled into vessels. Angiogenesis refers to the expansion and remodeling of the primitive vessels into a functional vascular network. In adults, angiogenesis is also involved in pathological conditions such as tumors, retinopathies and rheumatoid arthritis. The process of angiogenesis includes the branching of vessels into small capillaries, the sprouting of new vessels, and longitudinal division. In mature vessels, endothelial cells are surrounded by periendothelial cells, which are pericytes in small vessels and smooth muscle cells in large vessels, that stabilize the vessels. The search for inductors of vasculogenesis and angiogenesis led to the identification of several soluble factors, as well as matrix proteins which play an essential role. Positive and negative regulators of these processes regulate proliferation, migration, differentiation of endothelial cells, degradation of the extracellular matrix, and tube formation1–3.
Gastrointestinal bleeding in von Willebrand patients: special diagnostic and management considerations
Published in Expert Review of Hematology, 2023
Edwin Ocran, Nicholas L.J. Chornenki, Mackenzie Bowman, Michelle Sholzberg, Paula James
The formation and development of new blood vessels is a highly complex process involving several pathways and is achieved through two fundamental mechanisms, vasculogenesis and angiogenesis, which are essential for growth and repair of tissue. Vasculogenesis involves the differentiation of endothelial progenitor cells (EPCs), called angioblasts into endothelial cells, leading to the formation of a primordial vascular network [42]. Angiogenesis, on the other hand, involves the development of new capillaries from existing blood vessels and the remodeling and expansion of existing vascular networks [42]. Both vasculogenesis and angiogenesis play an important role during embryological development in utero. In adults, many physiological processes including wound healing and tissue repair are primarily through angiogenesis [43]. However, the recent identification of EPCs at sites of neurovascularization in animal models suggests that vasculogenesis plays a role in the development of blood vessels in the adult [44].
Barrier maintenance by S1P during inflammation and sepsis
Published in Tissue Barriers, 2021
Anke C. Ziegler, Markus H. Gräler
The importance of S1P signaling for the integrity of the vascular system was first demonstrated in S1P1−/- mice, which showed a major defect in the formation of blood vessels during embryogenesis.19 Vasculogenesis and angiogenesis are essential for blood vessel formation and maintenance. In vasculogenesis, new blood vessels are formed out of differentiated ECs. In angiogenesis, the new vascular system is stabilized by the differentiation of vascular smooth muscle cells (VSMCs) to cover new vessels.20–23 S1P1−/- mouse embryos died between week 12.5 and 14.5 because of severe bleeding,19 which occurred due to the incomplete coverage of the developed blood vessels by smooth muscle cells, leading to their instability and death of the embryos.20 Besides S1P1, additional deletion of S1P2 and S1P3 in double and triple knock-out mice increased the severity of the vascular phenotype, indicating cooperative functions of S1P receptors in vascular development.24
Isotretinoin does not alter VEGF-A and VEGF-C levels: do retinoids behave differently in dose-dependent and/or in vivo/in vitro conditions?
Published in Cutaneous and Ocular Toxicology, 2020
Erhan Ayhan, Eşref Araç, Özgür Aslan
Vascular endothelial growth factor (VEGF) family consists of VEGF-A (known as VEGF), VEGF-B, VEGF-C, VEGF-D and placental growth factor (PlGF). VEGF-A is an important regulator involved in the developmental vasculogenesis, angiogenesis and differentiation of progenitor endothelial cells. VEGF-B and PlGF induce angiogenesis in normal tissues, but their activity is much weaker than that of VEGF-A1,2. VEGF-C and VEGF-D are produced from their precursors and regulate lymphangiogenesis3,4. There are publications reporting that retinoids including isotretinoin (13-cis-retinoic acid) are successful in lymphangioma circumscriptum, angiolymphoid hyperplasia with eosinophilia, diffuse dermal angiomatosis, and Kaposi’s sarcoma5–12. In some publications, the effect of success is claimed to be the inhibitory effect on VEGF5,6. However, in the literature, it is seen that various forms of retinoids have different results on VEGF-A and VEGF-C levels when tested at different dosages, in different diseases and under different conditions such as in vivo or in vitro.13–18 However, there is no study on using only isotretinoin and its effect on VEGF-A and VEGF C in humans. Therefore, we aimed to investigate whether isotretinoin commonly used in dermatology has an effect on VEGF-A and VEGF-C.