Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.

https://science.sciencemag.org/content/sci/277/5323/242.full.pdf

Pericyte Loss and Microaneurysm Formation in PDGF-B-Deficient Mice

The association of pericytes (PCs) to newly formed blood vessels has been suggested to regulate endothelial cell (EC) proliferation, survival, migration, differentiation, and vascular branching. Here, we addressed these issues using PDGF-B– and PDGF receptor-β (PDGFR-β)–deficient mice as in vivo models of brain angiogenesis in the absence of PCs. Quantitative morphological analysis showed that these mutants have normal microvessel density, length, and number of branch points. However, absence of PCs correlates with endothelial hyperplasia, increased capillary diameter, abnormal EC shape and ultrastructure, changed cellular distribution of certain junctional proteins, and morphological signs of increased transendothelial permeability. Brain endothelial hyperplasia was observed already at embryonic day (E) 11.5 and persisted throughout development. From E 13.5, vascular endothelial growth factor-A (VEGF-A) and other genes responsive to metabolic stress became upregulated, suggesting that the abnormal microvessel architecture has systemic metabolic consequences. VEGF-A upregulation correlated temporally with the occurrence of vascular abnormalities in the placenta and dilation of the heart. Thus, although PC deficiency appears to have direct effects on EC number before E 13.5, the subsequent increased VEGF-A levels may further abrogate microvessel architecture, promote vascular permeability, and contribute to formation of the edematous phenotype observed in late gestation PDGF-B and PDGFR-β knock out embryos.

/pdf/lack-of-pericytes-leads-to-endothelial-hyperplasia-and-31xe2su2tc.pdf

Lack of pericytes leads to endothelial hyperplasia and abnormal vascular morphogenesis.

When a confluent monolayer of bovine aortic endothelial (BAE) cells is wounded with a razor blade, endothelial cells (ECs) spontaneously move into the denuded area. If bovine pericytes or smooth muscle cells (SMCs) are plated into the denuded area at low density, they block the movement of the ECs. This effect is dependent upon the number of cells plated into the wound area and contact between ECs and the plated cells. Antibodies to transforming growth factor-beta 1 (TGF-beta 1) abrogate the inhibition of BAE cell movement by pericytes or SMCs. TGF-beta 1, if added to wounded BAE cell monolayers, also inhibits cell movement. When cultured separately, BAE cells, pericytes, and SMCs each produce an inactive TGF-beta 1-like molecule which is activated in BAE cell-pericyte or BAE cell-SMC co-cultures. The activation appears to be mediated by plasmin as the inhibitory effect on cell movement in co-cultures of BAE cells and pericytes is blocked by the inclusion of inhibitors of plasmin in the culture medium.

/pdf/inhibition-of-endothelial-cell-movement-by-pericytes-and-1wl4v7kava.pdf

Inhibition of endothelial cell movement by pericytes and smooth muscle cells: activation of a latent transforming growth factor-beta 1-like molecule by plasmin during co-culture.

Vascular endothelial growth factors and angiogenesis in eye disease.

Regeneration and tissue repair processes consist of a sequence of molecular and cellular events which occur after the onset of a tissue lesion in order to restore the damaged tissue. The exsudative, proliferative, and extracellular matrix remodeling phases are sequential events that occur through the integration of dynamic processes involving soluble mediators, blood cells, and parenchymal cells. Exsudative phenomena that take place after injury contribute to the development of tissue edema. The proliferative stage seeks to reduce the area of tissue injury by contracting myofibroblasts and fibroplasia. At this stage, angiogenesis and reepithelialization processes can still be observed. Endothelial cells are able to differentiate into mesenchymal components, and this difference appears to be finely orchestrated by a set of signaling proteins that have been studied in the literature. This pathway is known as Hedgehog. The purpose of this review is to describe the various cellular and molecular aspects involved in the skin healing process.

http://www.scielo.br/pdf/abd/v91n5/0365-0596-abd-91-05-0614.pdf

Wound healing - A literature review.

Role of the pericyte in wound healing: An ultrastructural study☆

A comparative ultrastructural study of a case of hemangiopericytoma and one of glomus tumor is presented. The study revealed the hemangiopericytoma cells to be large with large irregular nuclei. The intercellular spaces are filled with light osmiophilic material resembling basement membrane. In the glomus tumor, two types of cells are identified. The more frequent cells are epithelioid smooth muscle cells with large ovoid nuclei and cytoplasm filled with fine filaments. The second type of cell is less frequent and is recognized as a mast cell. It is suggested that the release of mast cell granules plays an important role in the contraction of epithelioid smooth muscle and therefore controls the flow of blood in the glomus structure.

Ultrastructure of a hemangiopericytoma and a glomus tumor

The relationship of myoepithelial cells to epithelial cells in normal mammary gland and in various diseases of this organ were studied. The evidence suggests that myoepithelial cells play an important role in the formation of some benign and malignant tumors of the breast. The study also showed the presence of light and dark myoepithelial cells.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%28196806%2921%3A6%3C1137%3A%3AAID-CNCR2820210615%3E3.0.CO%3B2-U

Ultrastructure of myoepithelial cells in human mammary gland tumors

A case of fibrosarcoma in a male breast was studied with light and electron microscope. The study revealed a close morphologic similarity between the neoplastic cells and the fibroblasts. The neoplastic cells differ from normal fibroblasts in having increased number of cytoplasmic filaments and multiple nucleoli. These features were thought to be the result of neoplastic transformation. It is also thought that this neoplasm arose from the pectoral fascia.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%28196904%2923%3A4%3C891%3A%3AAID-CNCR2820230426%3E3.0.CO%3B2-Z

Ultrastructure of fibrosarcoma in a male breast

Six biopsies from 5 cases of treated and untreated mycosis fungoides were studied with the light and electron microscope. The study revealed the presence of a characteristic cell type in the skin lesions. The characteristic cells had large infolded nuclei, scant cytoplasm, and few organelles. Mitochondria were clustered in one region of the cytoplasm in which the Golgi apparatus was found. Treatment with systemic corticosteroids and electron beam therapy caused no significant change in the mycosis fungoides cells. Treatment with chemotherapy appeared to damage the malignant cells to a lesser extent than the surrounding cells. The combination of chemotherapy and x-irradiation caused smoothening of the nuclear envelope, vesiculation of the endoplasmic reticulum, mitochondrial swelling, and the appearance of membrane-bound lysosome-like bodies. These changes were seen in both the mycosis fungoides cells and in other cell types present in the cutaneous lesions. No method of treatment produced necrosis in the mycosis fungoides cells.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%28197009%2926%3A3%3C686%3A%3AAID-CNCR2820260330%3E3.0.CO%3B2-X

Tariq M. Murad

Papers

Role of the pericyte in wound healing: An ultrastructural study☆

Ultrastructure of a hemangiopericytoma and a glomus tumor

Ultrastructure of myoepithelial cells in human mammary gland tumors

Ultrastructure of fibrosarcoma in a male breast

Ultrastructure of mycosis fungoides.