Early Effects of Castration on the Vascular System of the Rat Ventral Prostate Gland*

Endocrinology ◽  
1999 ◽  
Vol 140 (4) ◽  
pp. 1920-1926 ◽  
Author(s):  
Ahmad Shabisgh ◽  
Nozomu Tanji ◽  
Vivette D’Agati ◽  
Martin Burchardt ◽  
Mark Rubin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Vascular System ◽  
Prostate Gland ◽  
Muscle Cells ◽  
Ventral Prostate ◽  
Morphological Evidence ◽  
Rat Ventral Prostate

Abstract Recent studies have found that blood flow to the rat ventral prostate gland is drastically reduced at an early time after castration. These observations caused us to reevaluate the effects of castration on the various cell populations of the ventral prostate, especially those in the prostatic vascular system. Sections of ventral prostate glands obtained at different times after castration were analyzed using the TUNEL (terminal deoxynucleotide transferase-mediated dUTP nick END labeling) staining method to quantify apoptosis in different cell types. The results of this analysis showed a significant increase in TUNEL staining of prostate endothelial and (nonendothelial) stromal cells as early as 12 h postcastration that continued to 24 h after castration. In contrast, TUNEL labeling of prostate epithelial cells was not significantly increased compared with control values until 72 h after castration. The use of dual immunohistochemical staining procedures (anti-CD31 for endothelial cells or antismooth muscle actin for smooth muscle cells combined with TUNEL labeling) allowed us to confirm that the TUNEL-positive vascular cells at these early times after castration were endothelial in nature, whereas smooth muscle cells surrounding the prostate glands or portions of the afferent vascular endothelium were rarely TUNEL labeled. Electron microscopic evaluation of ventral prostate tissues at 48 h after castration provided further morphological evidence for the occurrence of apoptosis in prostate endothelial cells. Finally, the Lendrum-Fraser histochemical procedure used to identify fibrin leakage in tissues with vascular damage was applied to sections of the ventral prostate gland. This stain revealed diffuse fibrin accumulation in periglandular areas outside the capillaries and blood vessels in prostates from 24-h castrated rats, but not in prostates of sham-operated rats. Our results confirm an early effect of castration on the vascular system of the rat ventral prostate identified by increased apoptosis of endothelial cells and vascular leakiness. As these changes temporally precede the loss of epithelial cells, we propose that they may be causal rather than incidental to regression of the rat ventral prostate after castration.

scholarly journals Seminal Vesicles and Bulbourethral Glands of Mammals: Morphology, Physiology, Ecology, Action of Extreme Destabilizing Factors

2021 ◽  
Vol 10 (3) ◽  
pp. 98-107
Author(s):  
N. N. Shevlyuk ◽  
M. F. Ryskulov
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Seasonal Pattern ◽  
Prostate Gland ◽  
Muscle Cells ◽  
Seminal Vesicles ◽  
Natural Ecosystems ◽  
Secretory Cycle

In mammals, the adnexal sex glands are represented by seminal vesicles, the prostate gland, urethral and bulbourethral glands, as well as glands that coagulate sperm and ampullary glands. The secret of the accessory genital glands increases the volume of the ejaculate (the share of secretions of these glands accounts for about 95% of the volume of ejaculate) promotes sperm, causes increased contraction of smooth muscle cells in the walls of the female genital tract.The purpose of this review is to analyze the morphofunctional organization of seminal vesicles and bulbourethral glands of mammalian animals and humans.The presence or absence of seminal vesicles is a species-specific feature. Among mammals, seminal vesicles are well developed in some rodents, insectivores, a number of domestic animals (cattle, pigs), and primates. These glands are absent in cloacae, marsupials, some carnivores, a number of insectivores, artiodactyls. Bulbourethral glands are well developed in rodents, bats, primates, and some ungulates.In the wall of the seminal vesicles, the mucous, muscular and outer membranes are isolated. The epithelium of the secretory parts is pseudomultitial, the interstitium is represented by loose fibrous connective tissue and a significant number of smooth muscle cells. In the wall of the bulbourethral glands, the mucosa and adventitial membrane are isolated. The secretory end sections of the bulbourethral glands are lined with a single-layer single-row epithelium, glandular cells produce a mucosal or mixed secret. The seminal vesicles and bulbourethral glands are androgen-dependent glands. In species with a seasonal pattern of reproduction, their morphofunctional characteristics undergo significant changes during the circannual rhythm of reproduction.The epithelium of seminal vesicles and bulbourethral glands is very sensitive to the action of various adverse factors (heavy metal compounds, organic xenobiotics, electromagnetic radiation, ultrasound, etc.). When exposed to various negative factors in the adnexal glands, a complex of changes occurs (edema of connective tissue and epithelium, decreased secretory activity of epithelial cells, desynchronization of the secretory cycle, desquamation of glandular epithelial cells, proliferation of interstitial connective tissue).There is a lack of information on many aspects of the characteristics of the adnexal glands of the male reproductive system, primarily on the morphology and physiology of the adnexal glands of animals in natural ecosystems, on the ultrastructural and immunohistochemical characteristics of these glands, as well as on the mechanisms of regulation of morphofunctional rearrangements of the adnexal glands during seasonal reproduction rhythms, in the conditions of adaptation to various negative influences.

Role of PDGF-B and PDGFR-beta in recruitment of vascular smooth muscle cells and pericytes during embryonic blood vessel formation in the mouse

Development ◽  
1999 ◽  
Vol 126 (14) ◽  
pp. 3047-3055 ◽  
Author(s):  
M. Hellstrom ◽  
M. Kal n ◽  
P. Lindahl ◽  
A. Abramsson ◽  
C. Betsholtz
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular System ◽  
Muscle Cells ◽  
Brdu Labeling ◽  
Pdgfr Beta

Development of a vascular system involves the assembly of two principal cell types - endothelial cells and vascular smooth muscle cells/pericytes (vSMC/PC) - into many different types of blood vessels. Most, if not all, vessels begin as endothelial tubes that subsequently acquire a vSMC/PC coating. We have previously shown that PDGF-B is critically involved in the recruitment of pericytes to brain capillaries and to the kidney glomerular capillary tuft. Here, we used desmin and alpha-smooth muscle actin (ASMA) as markers to analyze vSMC/PC development in PDGF-B−/− and PDGFR-beta−/− embryos. Both mutants showed a site-specific reduction of desmin-positive pericytes and ASMA-positive vSMC. We found that endothelial expression of PDGF-B was restricted to immature capillary endothelial cells and to the endothelium of growing arteries. BrdU labeling showed that PDGFR-beta-positive vSMC/PC progenitors normally proliferate at sites of endothelial PDGF-B expression. In PDGF-B−/− embryos, limb arterial vSMC showed a reduced BrdU-labeling index. This suggests a role of PDGF-B in vSMC/PC cell proliferation during vascular growth. Two modes of vSMC recruitment to newly formed vessels have previously been suggested: (1) de novo formation of vSMC by induction of undifferentiated perivascular mesenchymal cells, and (2) co-migration of vSMC from a preexisting pool of vSMC. Our data support both modes of vSMC/PC development and lead to a model in which PDGFR-beta-positive vSMC/PC progenitors initially form around certain vessels by PDGF-B-independent induction. Subsequent angiogenic sprouting and vessel enlargement involves PDGF-B-dependent vSMC/PC progenitor co-migration and proliferation, and/or PDGF-B-independent new induction of vSMC/PC, depending on tissue context.

scholarly journals Steroid-sensitive gene-1 is an androgen-regulated gene expressed in prostatic smooth muscle cells in vivo

2001 ◽  
Vol 26 (3) ◽  
pp. 175-184 ◽  
Author(s):  
D Marcantonio ◽  
LE Chalifour ◽  
MA Alaoui-Jamali And H T Huynh ◽  
MA Alaoui-Jamali ◽  
MA Alaoui-Jamali ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Muscle Cells ◽  
Ventral Prostate ◽  
Mrna Levels ◽  
Rat Ventral Prostate ◽  
Steroid Sensitive

Steroid-sensitive gene-1 (SSG1) is a novel gene we cloned, found regulated by 17beta-estradiol in the rat uterus and mammary gland, and over-expressed in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors. We show here that SSG1 mRNA and protein expression are regulated by androgens in the rat ventral prostate. Increases in SSG1 mRNA levels were detected by Northern blotting after 24 h and reached a 27-fold peak 96 h following castration, relative to SSG1 mRNA expression in sham-operated rats. Dihydrotestosterone or testosterone supplementation of castrated rats prevented this rise in SSG1 mRNA. In contrast with SSG1 mRNA expression, SSG1 protein was decreased 16-fold 2 weeks following castration but was at control levels in the prostates of castrated rats receiving dihydrotestosterone or testosterone. Although SSG1 is regulated by androgens in vivo, treatment of LnCap cells with dihydrotestosterone, cyproterone acetate or flutamide did not result in the regulation of SSG1 protein levels in vitro. Immunofluorescence studies show that SSG1 is mainly expressed in prostatic smooth muscle cells. These results indicate that SSG1 is an androgen-regulated gene that is expressed in the smooth muscle component of the rat ventral prostate in vivo.

scholarly journals Expression of PDE11A in Normal and Malignant Human Tissues

2005 ◽  
Vol 53 (7) ◽  
pp. 895-903 ◽  
Author(s):  
Michael R. D'Andrea ◽  
Yuhong Qiu ◽  
Donna Haynes-Johnson ◽  
Sheela Bhattacharjee ◽  
Patricia Kraft ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Intracellular Camp ◽  
Human Tissues ◽  
Physiological Processes ◽  
Wide Range ◽  
Human Carcinomas

Cyclic nucleotide phosphodiesterase 11A (PDE11A) is the newest member in the PDE family. Although the tissue distribution of PDE11A mRNA has been shown, its protein expression pattern has not been well studied. The goal of this report is to investigate the distribution of PDE11A proteins in a wide range of normal and malignant human tissues. We utilized a polyclonal antibody that recognized all four PDE11A isoforms. Its specificity was demonstrated by Western blot analysis on a recombinant human PDE11A protein and native PDE11A proteins in various human tissues. Immunohistochemistry showed that PDE11A is widely expressed. Various degrees of immunoreactivity were observed in the epithelial cells, endothelial cells, and smooth muscle cells of all tissues examined. The highest expression was in the epithelial, endothelial, and smooth muscle cells of the prostate, Leydig, and spermatogenic cells of the testis, the tubule epithelial cells in the kidney, the epithelial and endothelial cells in the adrenal, the epithelial cells and macrophages in the colon, and the epidermis in the skin. Furthermore, PDE11A expression was also detected in several human carcinomas. Our results suggest that PDE11A might be involved in multiple physiological processes in various organs via its ability to modulate intracellular cAMP and cGMP levels.

scholarly journals ACE2/Ang-(1-7)/Mas1 axis and the vascular system: vasoprotection to COVID-19-associated vascular disease

2021 ◽  
Vol 135 (2) ◽  
pp. 387-407
Author(s):  
Jithin Kuriakose ◽  
Augusto C. Montezano ◽  
Rhian M. Touyz
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cardiovascular Health ◽  
Vascular System ◽  
Prognostic Significance ◽  
Muscle Cells ◽  
Ang Ii ◽  
Enzymatic Function

Abstract The two axes of the renin–angiotensin system include the classical ACE/Ang II/AT1 axis and the counter-regulatory ACE2/Ang-(1-7)/Mas1 axis. ACE2 is a multifunctional monocarboxypeptidase responsible for generating Ang-(1-7) from Ang II. ACE2 is important in the vascular system where it is found in arterial and venous endothelial cells and arterial smooth muscle cells in many vascular beds. Among the best characterized functions of ACE2 is its role in regulating vascular tone. ACE2 through its effector peptide Ang-(1-7) and receptor Mas1 induces vasodilation and attenuates Ang II-induced vasoconstriction. In endothelial cells activation of the ACE2/Ang-(1-7)/Mas1 axis increases production of the vasodilator’s nitric oxide and prostacyclin’s and in vascular smooth muscle cells it inhibits pro-contractile and pro-inflammatory signaling. Endothelial ACE2 is cleaved by proteases, shed into the circulation and measured as soluble ACE2. Plasma ACE2 activity is increased in cardiovascular disease and may have prognostic significance in disease severity. In addition to its enzymatic function, ACE2 is the receptor for severe acute respiratory syndrome (SARS)-coronavirus (CoV) and SARS-Cov-2, which cause SARS and coronavirus disease-19 (COVID-19) respectively. ACE-2 is thus a double-edged sword: it promotes cardiovascular health while also facilitating the devastations caused by coronaviruses. COVID-19 is associated with cardiovascular disease as a risk factor and as a complication. Mechanisms linking COVID-19 and cardiovascular disease are unclear, but vascular ACE2 may be important. This review focuses on the vascular biology and (patho)physiology of ACE2 in cardiovascular health and disease and briefly discusses the role of vascular ACE2 as a potential mediator of vascular injury in COVID-19.

Collagen fiber reorganization in the rat ventral prostate following androgen deprivation: A possible role for smooth muscle cells

The Prostate ◽  
2000 ◽  
Vol 45 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Patr�cia S.L. Vilamaior ◽  
S�rgio L. Felisbino ◽  
Sebasti�o R. Taboga ◽  
Hernandes F. Carvalho
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Collagen Fiber ◽  
Muscle Cells ◽  
Androgen Deprivation ◽  
Ventral Prostate ◽  
Rat Ventral Prostate

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

1994 ◽  
Vol 72 (01) ◽  
pp. 044-053 ◽  
Author(s):  
N Chomiki ◽  
M Henry ◽  
M C Alessi ◽  
F Anfosso ◽  
I Juhan-Vague
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Human Liver ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Vessel Walls ◽  
Activator Inhibitor ◽  
Pai 1

SummaryIndividuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization.We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states.In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

1982 ◽  
Vol 48 (01) ◽  
pp. 101-103 ◽  
Author(s):  
B Kirchhof ◽  
J Grünwald
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vessel Wall ◽  
Thrombin Generation ◽  
Muscle Cells ◽  
Thrombin Inhibition ◽  
Generating Capacity ◽  
Wall Interaction ◽  
Cells Cultured

SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.

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