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1 ssed by melanocytes, dermal fibroblasts, and dermal microvascular endothelial cells.
2 ramatic increase in adhesion of IEs to human dermal microvascular endothelial cells.
3 1 (ICAM-1), and E-selectin in cultured human dermal microvascular endothelial cells.
4 nol-treated LSEC from control rats and human dermal microvascular endothelial cells.
5 hanol treatment of isolated rLSECs and human dermal microvascular endothelial cells.
6 d the formation of spindle cells and foci of dermal microvascular endothelial cells.
7 t productive macropinocytic entry into human dermal microvascular endothelial cells.
8 angiogenesis assays were performed in human dermal microvascular endothelial cells.
9 C3a, was chemotactic for human immortalized dermal microvascular endothelial cells.
10 rating how activation of telomerase in human dermal microvascular endothelial cells affects their dur
12 AP) caused G(1)/S cell cycle arrest in human dermal microvascular endothelial cells and also induced
14 ial growth factor induced migration of human dermal microvascular endothelial cells and inhibited tub
15 Moreover, TSP-2/NTF potently induced human dermal microvascular endothelial cell apoptosis in vitro
16 cytokine-stimulated human umbilical vein and dermal microvascular endothelial cells as substrates, re
18 and it also inhibits the migration of human dermal microvascular endothelial cells at similar concen
19 he proliferation of human umbilical vein and dermal microvascular endothelial cells, but did not affe
20 aspase death pathway in both HUVEC and human dermal microvascular endothelial cells, but only activat
21 as anti-angiogenic effect on human brain and dermal microvascular endothelial cells co-cultured with
22 the ability to arrest on TNF-alpha activated dermal microvascular endothelial cells compared with nor
24 mulate the in vivo environment better, human dermal microvascular endothelial cells cultured on colla
26 expressed by human keratinocytes and not by dermal microvascular endothelial cells, dermal fibroblas
27 in human keratinocytes nor induced in human dermal microvascular endothelial cells, dermal fibroblas
28 ansfected 293 cells (293/VEGFR-3) or primary dermal microvascular endothelial cells (DMEC), we found
30 and 293T cells or adenovirus vGCR-transduced dermal microvascular endothelial cells (DMVEC) as detect
32 cell lines can induce cultured primary human dermal microvascular endothelial cells (DMVEC) to form c
34 n can be replicated in vitro by infection of dermal microvascular endothelial cells (DMVEC) with KSHV
36 ch more efficient at infecting primary human dermal microvascular endothelial cells (DMVECs) with KSH
37 nical forms of KS, and in vitro infection of dermal microvascular endothelial cells (DMVECs) with KSH
38 asculature formation, and migration of db/db dermal microvascular endothelial cells (DMVECs), as well
40 n umbilical vein endothelial cells and human dermal microvascular endothelial cells each became marke
42 is study, we describe their effects on human dermal microvascular endothelial cells (ECs), a natural
44 we found that HUVECs and immortalized human dermal microvascular endothelial cells express small num
45 st cells (HMC-1) and their products on human dermal microvascular endothelial cell (HDMEC) tube forma
46 ides on the expression and function of human dermal microvascular endothelial cell (HDMEC) VCAM-1.
47 r mTC to arrest on TNF-alpha-activated human dermal microvascular endothelial cells (HDMEC) in vitro
48 ot naive T cells respond to allogeneic human dermal microvascular endothelial cells (HDMEC) in vitro
49 e expression of E-selectin on cultured human dermal microvascular endothelial cells (HDMEC) isolated
50 aining human keratinocytes, fibroblasts, and dermal microvascular endothelial cells (HDMEC) isolated
52 he mechanisms mediating the binding of human dermal microvascular endothelial cells (HDMEC) to immobi
53 inase (SMase) rapidly (1 h) sensitized human dermal microvascular endothelial cells (HDMEC) to the cy
54 arrest of a subset of mTC to activated human dermal microvascular endothelial cells (HDMEC) under phy
56 alpha-induced VCAM-1 gene expression, human dermal microvascular endothelial cells (HDMEC) were stim
57 s of E-selectin expression on cultured human dermal microvascular endothelial cells (HDMEC) with expr
58 Persistent E-selectin expression on human dermal microvascular endothelial cells (HDMEC), believed
62 nditioned medium from Bcl-2-transduced human dermal microvascular endothelial cells (HDMEC-Bcl-2) is
63 ficantly superior to that generated by human dermal microvascular endothelial cells (HDMECs) but simi
64 s in vivo and prolongs the survival of human dermal microvascular endothelial cells (HDMECs) in vitro
65 e investigated the mechanisms by which human dermal microvascular endothelial cells (HDMECs) perceive
67 gamma-Irradiation-induced apoptosis of human dermal microvascular endothelial cells (HDMECs) was pred
70 esis, we have studied their effects on human dermal microvascular endothelial cell (HDMVEC) tube form
71 enic, we have studied their effects on human dermal microvascular endothelial cell (HDMVEC) tube form
79 ibroblast growth factor (bFGF)-induced human dermal microvascular endothelial cell (HMVEC) chemotaxis
80 at sE-selectin is a potent mediator of human dermal microvascular endothelial cell (HMVEC) chemotaxis
81 f Kaposi's sarcoma, we studied primary human dermal microvascular endothelial cells (HMVEC) exposed t
83 vely, keratinocytes, dermal fibroblasts, and dermal microvascular endothelial cells (HMVEC-d) all sup
84 ption of several host genes of primary human dermal microvascular endothelial cells (HMVEC-d) and fib
85 uring the early stages of infection of human dermal microvascular endothelial cells (HMVEC-d) and hum
86 and in vitro KSHV infection of primary human dermal microvascular endothelial cells (HMVEC-d) is char
87 ta5) and associated signaling to enter human dermal microvascular endothelial cells (HMVEC-d), an in
88 a-associated herpesvirus (KSHV) enters human dermal microvascular endothelial cells (HMVEC-d), its na
90 oma-associated herpesvirus (KSHV) into human dermal microvascular endothelial cells (HMVEC-d), natura
91 on of primary human endothelial [human adult dermal microvascular endothelial cells (HMVECd)] and for
92 gnificantly enhanced the expression of human dermal microvascular endothelial cells (HMVECs) intercel
93 MIF-induced adhesion of HL-60 cells to human dermal microvascular endothelial cells (HMVECs) or an en
94 rd vein endothelial cells (HUVECs) and human dermal microvascular endothelial cells (HMVECs) were per
95 fkn significantly induced migration of human dermal microvascular endothelial cells (HMVECs), a facet
96 tion and tube formation in Matrigel of human dermal microvascular endothelial cells (HMVECs), with po
97 egulation of alphavbeta3 expression on human dermal microvascular endothelial cells, however, have no
98 roteins in cultured human umbilical vein and dermal microvascular endothelial cells (HUVEC and HDMEC,
101 nduction with supernatant derived from human dermal microvascular endothelial cells, isolated lymphat
105 radiolabeled recombinant mouse C5a to mouse dermal microvascular endothelial cells (MDMEC) with a K(
110 levels of alphav/beta3 were higher in human dermal microvascular endothelial cells on fibronectin an
111 of immunomodulatory proteins on both primary dermal microvascular endothelial cells (pDMVEC) infected
112 GF- and histamine-induced increases in human dermal microvascular endothelial cell permeability in vi
114 ession of KSHV gB on as few as 1-2% of human dermal microvascular endothelial cells resulted in a 10-
115 biodegradable scaffolds to co-implant human dermal microvascular endothelial cells stably expressing
116 lphav/beta3 mRNA levels were higher in human dermal microvascular endothelial cells surrounded by a t
118 mide pretreatment enabled immortalized human dermal microvascular endothelial cells that have lost th
119 e have developed an in vitro model utilizing dermal microvascular endothelial cells that support sign
120 is the major entry pathway of KSHV in human dermal microvascular endothelial cells, the natural targ
121 n umbilical vein endothelial cells and human dermal microvascular endothelial cells, the NO donor die
122 ther inflammatory mediators by primary human dermal microvascular endothelial cells through a signali
123 G significantly reduced the ability of human dermal microvascular endothelial cells to form a capilla
124 results show that neutrophils traverse human dermal microvascular endothelial cells using one of two
125 eta3, and alphavbeta5 integrins each support dermal microvascular endothelial cell viability, and tha
126 mediated virus reactivation in KSHV-infected dermal microvascular endothelial cells was blocked by cy
127 luR1), mGluR4, and mGluR5 by human brain and dermal microvascular endothelial cells was demonstrated
128 eron regulatory factor-1 expression in human dermal microvascular endothelial cells was transcription
131 an umbilical vein endothelial cells or adult dermal microvascular endothelial cells were transduced w
132 ntacts in confluent cultured human renal and dermal microvascular endothelial cells, yet experimental
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