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Table 1 Effects of androgens on functions of the cerebral vasculature

From: Androgens’ effects on cerebrovascular function in health and disease

Function

Subjects/cells

Androgen

Results

Reference

Angiogenesis

EPC (healthy male donors)

Methyltrienolone (synthetic androgen)

Dose-dependent increase in proliferation, migration and colony formation. Effect is AR-dependent (blocked by flutamide).

Foresta et al. [29]

Angiogenesis

EPC (healthy male donors)

DHT

Dose- and time-dependent increase in VEGF and proliferative, migratory, and adhesive abilities of EPCs. Via RhoA/ROCK pathway.

Zhang et al. [30]

Angiogenesis

EPC (healthy male donors)

DHT

Dose- and time-dependent increase in proliferative activity and adhesive ability of EPCs. The PI3-K/Akt pathway plays a role.

Liu et al. [31]

Angiogenesis

Healthy adult males

N/A

T/E2 ratio negatively correlated with number of EPCs.

Fadini et al. [32]

Angiogenesis

EPC (healthy male donors)

T or DHT

No effect on expansion and function of late EPCs; increase generation of early EPCs

Fadini et al. [32]

Angiogenesis

Adult male SD rats (intact & GDX)

T or DHT replacement

T & DHT replacement unable to restore reduced EPC levels in GDX males

Fadini et al. [32]

Angiogenesis

Adult female canaries

T

Increased angiogenesis and endothelial BDNF, VEGF, and VEGF-R in the brain

Louissaint et al. [33]

Cerebrovascular reactivity

Adult male Fisher 344 rats (intact & GDX)

T replacement

Endothelium-dependent myogenic tone is reduced in GDX rats, which is NOS-independent and reversed by T replacement.

Geary et al. [34]

Cerebrovascular reactivity

Adult male Fisher 344 rats (GDX)

T replacement

T replacement increased vascular tone in endothelium-dependent manner of isolated MCA, independent of COX, NOS, and endothelin. Effect may be through suppression of EDHF-like vasodilator.

Gonzales et al. [35]

Cerebrovascular reactivity

Adult male Fisher 344 rats (GDX)

T replacement

T replacement increased vascular tone of MCA, likely by increasing synthesis of thromboxane A2.

Gonzales et al. 2005 [36]

BBB function and inflammation

Adult male C57BL/6J mice (intact & GDX)

T replacement

GDX increased BBB permeability and inflammation; reduced EC TJ proteins. Effects reversed by T replacement.

Atallah et al. [37]

Blood-spinal cord barrier

Young adult male Wistar rats

T

T treatment decreased some TJ proteins in spinal cord and increased P-gp expression.

Nierwinska et al. [38]

Inflammation

Adult male Wistar rats (GDX)

DHT replacement

DHT stimulated CBV inflammation by increasing COX-2, iNOS, and NFkB levels in cerebral arteries (ex vivo and in vivo). Effect is AR-dependent (blocked by flutamide).

Gonzales et al. [39]

Inflammation

Adult male Wistar rats (GDX)

DHT (in vivo or ex vivo)

DHT increases COX-2 under normoxia but decreases COX-2 under hypoxia in cerebral arteries. DHT blunts HIF-1a following hypoxia.

Zuloaga & Gonzales [40]

Inflammation

Primary human brain VSMC

DHT

DHT increases COX-2 under normoxia but decreases COX-2 under hypoxia. DHT blunts HIF-1a following hypoxia (AR-independent).

Zuloaga & Gonzales [40]

Inflammation

Primary human brain VSMC

DHT

Anti-inflammatory effect of DHT (reduction of COX-2) is mediated by ER-beta, likely via conversion to 3β-diol

Zuloaga et al. [22]

Inflammation

Adult male Fisher 344 rats (intact & GDX)

T (in vivo) or ex vivo T treatment

T increases LPS-induced CBV inflammation (COX-2, iNOS, PGE2).

Razmara et al. [41]

EC senescence

Adult male SAMP8, control SAMR 1 mice

DHT

DHT treatment decreases hippocampal endothelial cell senescence.

Ota et al. [42]