Cell-mediated and neural control of morphostasis

Bukovský, Antonín; Michael, S.D.; Presl, J

doi:10.1016/0306-9877(91)90146-p

Cited by 28 publications

(29 citation statements)

References 21 publications

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“…Why growing and degenerating small antral follicles differ in thecal development is a matter for speculation. Factors controlling thecal development are complex and may operate via autonomic innervation associated with thecal vessels [42]. It has been reported that ovarian nerve extracts influence thecal androgen production [43,44].…”

Section: Discussionmentioning

confidence: 99%

“…Macrophages are known to migrate through basal lamina into various epithelial tissues (e.g., gut, epidermis, ectocervix, oviduct, and vagina [42,53,54]) and also into developing [55] and mature [56] follicles. Considering that immune cells produce many peptide hormones, including hCG, upon antigenic stimulation [57,58], we propose that macrophages are attracted by chemotaxis, enter preantral follicles, and prime the oocyte/cumulus complex through cellcell communication [59][60][61].…”

Section: Discussionmentioning

confidence: 99%

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Cellular Localization of Luteinizing Hormone Receptor Immunoreactivity in the Ovaries of Immature, Gonadotropin-Primed and Normal Cycling Rats1

Bukovský

Chen

Wimalasena

et al. 1993

Biology of Reproduction

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In this study we used two monoclonal antibodies against purified LH receptor (LHR) to localize and quantify LHR in ovarian compartments during follicular development, using gonads from immature, gonadotropin-primed, and normal cycling rats. In early preantral follicles, LHR immunoreactivity (LHRI) was identified in vascular endothelium and subsequently appeared in vascular pericytes. In healthy small antral (200-550-microns) follicles, LHRI continued to be present in thecal pericytes, but not in cells of the theca interna. However, in small antral follicles undergoing atresia, a dramatic decrease in thecal vessel LHRI with a concomitant increase in LHRI in hypertrophied theca was observed. In healthy antral follicles, LHRI of thecal cells was not observed until the cells reached medium (550-microns) size. High LHRI was occasionally observed in macrophage-like cells adjacent to the oocyte of large preantral follicles and among granulosa layers of medium-sized antral follicles. In the membrana granulosa, LHRI first appeared in cumulus cells of medium-sized antral follicles and subsequently spread to the entire granulosa cell population of large (750 microns) antral follicles. Treatment of immature rats with eCG markedly enhanced LHRI in theca and granulosa cells of all antral follicles, while eCG/hCG-treated (pseudopregnant) rats showed lack of LHRI in follicles and interstitial glands, but not in corpora lutea (CL). Within degenerating CL in the cycling ovary, compared to fresh and mature CL, a significant decrease occurred in intracellular LHRI. Our observations indicate that 1) vascular pericytes may play a role in follicular development; 2) LHR expression in granulosa may require an interaction of macrophages, oocytes, and cumulus cells; and 3) thecal hypertrophy accompanied by enhanced LHR expression occurs on follicles undergoing atresia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cellular Localization of Luteinizing Hormone Receptor Immunoreactivity in the Ovaries of Immature, Gonadotropin-Primed and Normal Cycling Rats1

Bukovský

Chen

Wimalasena

et al. 1993

Biology of Reproduction

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“…It has been proposed that the luteal cells therefore represent immunologically unique cells [14]. Luteal cells in the CL of menstruation may be forced into metabolic inactivity (senescence) and morphologic regression by immune system-related molecules and cells [14]. Macrophages and lymphocytes have been morphologically detected in the regressing human CL [18,19].…”

Section: Introductionmentioning

confidence: 98%

“…In large mammals, including primates, immune adaptation occurs during intrauterine life [17]. It has been proposed that the luteal cells therefore represent immunologically unique cells [14]. Luteal cells in the CL of menstruation may be forced into metabolic inactivity (senescence) and morphologic regression by immune system-related molecules and cells [14].…”

Section: Introductionmentioning

confidence: 99%

“…Small blood vessels are accompanied by Thy-l-positive pericytes [5,6], which may enhance proliferation and preservation of endothelial cells [7]. Thy-1 differentiation protein accompanies differentiation and regeneration of parenchymal cells in various tissues, in vivo [8][9][10][11][12] and in vitro [13], and may be important in the maturation of luteal cells [14]. Additionally, the release of Thy-1 differentiation protein from vascular pericytes has recently been shown to accompany differentiation of human ovarian follicles [15,16].…”

Section: Introductionmentioning

confidence: 99%

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Is Corpus Luteum Regression an Immune-Mediated Event? Localization of Immune System Components and Luteinizing Hormone Receptor in Human Corpora Lutea1

Bukovský

Caudle

Keenan

et al. 1995

Biology of Reproduction

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Factors determining the life span of the human corpus luteum (CL) are not known. In addition to being determined by hormonal factors, such as hCG, the life of luteal cells may be determined by the preservation of luteal vascularization. Furthermore, the CL represents an immunologically unique tissue, as it is formed after menarche, long after adaptation of the immune system toward self. Thus, CL regression may be immunologically mediated. To determine what role the vasculature and immune system play in human CL development and regression, we examined immunohistochemically 1) the expression of Thy-1 differentiation protein by vascular pericytes, 2) the expression of major histocompatibility complex (MHC) class I and class II molecules in granulosa lutein cells (GLC), and 3) infiltration of the CL by macrophages and T lymphocytes. LH receptor (LHR) and cytokeratin 18 expression were also studied. In developing CL, the pericytes of luteal microvasculature released Thy-1 differentiation protein among the endothelial cells of proliferating vessels. In mature CL, Thy-1 released from vascular pericytes accumulated on the surface of GLC, and these cells exhibited LHR immunoreactivity (LHRI). Overall LHRI increased during the luteal phase and was strongest at the beginning of the late luteal phase. Although vascular pericytes showed strong LHRI, no staining of endothelium was detected during the luteal phase. GLC exhibited strong cytokeratin staining and moderate staining for MHC class I and MHC class II antigens; numerous macrophages were detected in luteal tissue. During pregnancy, the staining pattern was similar to that seen in the mature CL at the end of the midluteal phase. During the late luteal phase, surface expression of MHC class I and MHC class II antigens by GLC was substantially enhanced, and some T cells invaded among luteal cells. By the end of the cycle, an acute regression of vasculature and luteal tissue was observed along the fibrous septa. The remaining GLC showed only surface and no cytoplasmic LHRI. During the subsequent cycle, in the presence of numerous T cells, regressing GLC exhibited strong surface expression of various macrophage markers, such as CD4, CD14, CD68, and leukocyte common antigen, a feature not detected in the CL during the luteal phase nor described in other tissues. A complete loss of cytokeratin staining in GLC was observed. In regressing CL, strong LHRI was present in the endothelium of small and large luteal vessels. In conclusion, vascular pericytes and macrophages may stimulate the development and senescence of luteal tissue. The senescence of GLC may be inconsistent with preservation of luteal vasculature, and T lymphocytes appear to participate in terminal regression of the CL. Regression of luteal tissue therefore resembles immunologic rejection of a transplant. During pregnancy, the aging process of GLC appears to be interrupted, possibly due to the temporary acceptance of the CL "graft."

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Mammalian Neo‐Oogenesis from Ovarian Stem CellsIn VivoandIn Vitro

Bukovský

Caudle

2014

Cell and Molecular Biology and Imaging of Stem Cells

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Cell-mediated and neural control of morphostasis

Cited by 28 publications

References 21 publications

Cellular Localization of Luteinizing Hormone Receptor Immunoreactivity in the Ovaries of Immature, Gonadotropin-Primed and Normal Cycling Rats1

Cellular Localization of Luteinizing Hormone Receptor Immunoreactivity in the Ovaries of Immature, Gonadotropin-Primed and Normal Cycling Rats1

Is Corpus Luteum Regression an Immune-Mediated Event? Localization of Immune System Components and Luteinizing Hormone Receptor in Human Corpora Lutea1

Mammalian Neo‐Oogenesis from Ovarian Stem CellsIn VivoandIn Vitro

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