Several recently identified proteins such as Bcl-2 and Bcl-x have been
found to regulate programmed cell death (ie, apoptosis). In this repo
rt, we examined the levels of expression of proteins that can either p
revent apoptosis (ie, Bcl-2 or he long form of Bcl-x, designated Bcl-x
(L)) or promote apoptosis (ie, Bax or the short form of Bcl-x, designa
ted Bcl-x(s)) in proliferating benign and malignant endothelial cells
(Ecs). In normal skin with quiescent ECs, no detection by immunohistoc
hemical staining wa observed for Bcl-x(L), Bcl-x(s), or Bcl-2. However
, in diseased skin samples that feature a prominent angiogenic respons
e such as in psoriasis or pyogenic granulomas, the proliferating ECs m
arkedly overexpressed Bcl-x(L), with little to no Bcl-2. IN an acquire
d-immune-deficiency-syndrome-related neoplasm, Kaposi's sarcoma, the s
pindle-shaped tumor cells also overexpressed Bcl-x(L) compared with Bc
l-2. These in vivo studies were extended in vitro using cultured ECs a
nd kaposi's sarcoma tumor cells that were examined by flow cytometry a
nd immunoblot analysis. Both cultured ECs and Kaposi's sarcoma tumor c
ells express significantly higher levels of Bcl-x(L) than Bcl-2. Such
overexpression of cell survival gene products may contribute to prolon
ging the longevity of EC-derived cells in several different benign and
neoplastic skin disorders that are characterized by a prominent angio
genic tissue response.