CD34 expression is regulated reciprocally with adhesion molecules in vascular endothelial cells in vitro

Abstract

Freshly cultured vascular endothelial cells express the CD34 antigen in a diffuse cell surface pattern with some concentration on microvilli. Expression is downregulated with proliferation in continuous culture and undetectable after nine population doublings but can be maintained by restraining cell proliferation and promoting cell contact. Expression of CD34 at the antigen and mRNA levels on early passage cells is rapidly downregulated by interleukin-1 beta (IL-1 beta), interferon-gamma (INF-gamma), and tumor necrosis factor-alpha (TNF- alpha) under conditions in which these ligands upregulate the adhesion molecules: endothelial leukocyte adhesion molecule 1 (ELAM-1) and intracellular adhesion molecule 1 (ICAM-1). This reciprocal pattern of expression and the topographic distribution of CD34 molecules on the lumenal interdigitated microprocesses of adjacent endothelial cells in vivo suggest that CD34 might have a negative modulating role on adhesion functions of endothelia.

Expression of VCAM‐1, ICAM‐1, E‐ and P‐selectin and tumour‐associated macrophages in renal cell carcinoma

“…This might be due to a suppressed in¯ammatory response of microvessels under growth factor stimuli, to an increased shedding of adhesion molecules or to a switch towards the expression of soluble adhesion molecule isoforms. 5±9 In contrast to the in vitro experiments of Delia et al 13 we did not ®nd a coordinated downregulation of CD34 and upregulation of ICAM-1 in situ. The association of macrophage in®ltration with high ICAM-1 and VCAM-1 expression on tumour epithelia may be due to macrophage or lymphocyte-derived cytokines such as TNF-a or interferon-g. 8 However, the association of high ICAM-1 and VCAM-1 expression, a dense macrophage in®ltrate and minor grade of tumour differentiation does not argue for an effective function of ICAM-1 in the anti-tumour immune response as supposed by others.…”

Endothelial cell spheroids as a versatile tool to study angiogenesisin vitro

“…Because of their availability, easy preparation, and remarkable growth capacity (23), this cell type forms the in vitro backbone of vascular research. However, they gradually lose their original phenotype if maintained in standard 2-dimensional cell culture (24), and their responses may be biased by a plethora of exogenous factors. As HUVECs are isolated from umbilical cords, their phenotype may be affected from fetal distress, pregnancy-associated diseases such as preeclampsia, and any medication of the donors.…”

VEGF‐R blockade causes endothelial cell apoptosis, expansion of surviving CD34+precursor cells and transdifferentiation to smooth muscle‐like and neuronal‐like cells

“…In clinical practice CD34 is used as a marker for leukemia diagnosis and subclassification, as a label for the quantity of stem/progenitor cells in blood and marrow and also for purification of stem/progenitor cells for clinical transplantation (56,57). CD34 is up-regulated in vivo during angiogenesis (58) and is primarily expressed by small or newly formed vessels (59), whereas EC of larger veins, placenta, and lymphatic tissue are CD34negative (59). CD34 was reported to be expressed in alveolar capillaries rather than in large pulmonary vessels (60).…”