Angiogenesis in mice with chronic airway inflammation - Strain-dependent differences

被引:137
作者
Thurston, G
Murphy, TJ
Baluk, P
Lindsey, JR
McDonald, DM
机构
[1] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA
[3] Univ Alabama, Dept Comparat Med, Birmingham, AL 35294 USA
关键词
D O I
10.1016/S0002-9440(10)65654-4
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Chronic inflammation is associated with blood vessel proliferation and enlargement and changes in vessel phenotype. We sought to determine whether these changes represent different typos of angiogenesis and whether they are stimulus dependent. Chronic airway inflammation, produced by infection with Mycoplasma pulmonis, was compared in strains of mice known to be resistant (C57BL/6) or susceptible (C3H). Tracheal vascularity, assessed in whole mounts after Lycopersicon esculentum lectin staining, increased in both strains at 1, 2, 4, and 8 weeks after infection, but the type of vascular remodeling was different. The number of vessels doubled in tracheas of C57BL/6 mice, with corresponding increases of capillaries and venules, In contrast, neither the number nor the length of vessels changed in C3H mice. Instead, vessel diameter and endothelial cell number doubled, and the proportion of venules doubled with a corresponding decrease of capillaries. Although the infection had no effect on baseline plasma leakage, in both strains it potentiated the leakage produced by substance P. We conclude that the same stimulus can result in blood vessel proliferation or enlargement, depending on the host response. Endothelial cells proliferate in. both cases, but in one case new capillaries form whereas in the other capillaries convert to venules.
引用
收藏
页码:1099 / 1112
页数:14
相关论文
共 46 条
[1]   Vascular bed-specific expression of an endothelial cell gene is programmed by the tissue microenvironment [J].
Aird, WC ;
Edelberg, JM ;
WeilerGuettler, H ;
Simmons, WW ;
Smith, TW ;
Rosenberg, RD .
JOURNAL OF CELL BIOLOGY, 1997, 138 (05) :1117-1124
[2]   Isolation of putative progenitor endothelial cells for angiogenesis [J].
Asahara, T ;
Murohara, T ;
Sullivan, A ;
Silver, M ;
vanderZee, R ;
Li, T ;
Witzenbichler, B ;
Schatteman, G ;
Isner, JM .
SCIENCE, 1997, 275 (5302) :964-967
[3]  
BACHARACHBUHLES M, 1994, J INVEST DERMATOL, V103, P263
[4]   Upregulation of substance P receptors in angiogenesis associated with chronic airway inflammation in rats [J].
Baluk, P ;
Bowden, JJ ;
Lefevre, PM ;
McDonald, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 273 (03) :L565-L571
[5]   Endothelial gaps: Time course of formation and closure in inflamed venules of rats [J].
Baluk, P ;
Hirata, A ;
Thurston, G ;
Fujiwara, T ;
Neal, CR ;
Michel, CC ;
McDonald, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 272 (01) :L155-L170
[6]  
BARTON SP, 1992, BRIT J DERMATOL, V126, P569
[7]   DIRECT OBSERVATION OF SUBSTANCE-P-INDUCED INTERNALIZATION OF NEUROKININ-1 (NK1) RECEPTORS AT SITES OF INFLAMMATION [J].
BOWDEN, JJ ;
GARLAND, AM ;
BALUK, P ;
LEFEVRE, P ;
GRADY, EF ;
VIGNA, SR ;
BUNNETT, NW ;
MCDONALD, DM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (19) :8964-8968
[8]   Neurogenic amplification of immune complex inflammation [J].
Bozic, CR ;
Lu, B ;
Hopken, UE ;
Gerard, C ;
Gerard, NP .
SCIENCE, 1996, 273 (5282) :1722-1725
[9]   ROLE OF THE MICRO-CIRCULATION IN THE TREATMENT AND PATHOGENESIS OF PSORIASIS [J].
BRAVERMAN, IM ;
SIBLEY, J .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1982, 78 (01) :12-17
[10]   ULTRASTRUCTURE OF CAPILLARY LOOPS IN DERMAL PAPILLAE OF PSORIASIS [J].
BRAVERMAN, IM ;
YEN, A .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1977, 68 (01) :53-60