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1.
Biol Reprod ; 86(5): 155, 1-10, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22262689

RESUMO

In the seminiferous epithelium, spermatogonial stem cells (SSCs) are located in a particular environment called the "niche" that is controlled by the basement membrane, key testis somatic cells, and factors originating from the vascular network. However, the role of Leydig cells (LCs) as a niche component is not yet clearly elucidated. Recent studies showed that peccaries (Tayassu tajacu) present a peculiar LC cytoarchitecture in which these cells are located around the seminiferous tubule lobes, making the peccary a unique model for investigating the SSC niche. This peculiarity allowed us to subdivide the seminiferous tubule cross-sections in three different testis parenchyma regions (tubule-tubule, tubule-interstitium, and tubule-LC contact). Our aims were to characterize the different spermatogonial cell types and to determine the location and/or distribution of the SSCs along the seminiferous tubules. Compared to differentiating spermatogonia, undifferentiated spermatogonia (A(und)) presented a noticeably higher nuclear volume (P < 0.05), allowing an accurate evaluation of their distribution. Immunostaining analysis demonstrated that approximately 93% of A(und) were GDNF receptor alpha 1 positive (GFRA1(+)), and these cells were preferentially located adjacent to the interstitial compartment without LCs (P < 0.05). The expression of colony-stimulating factor 1 was observed in LCs and peritubular myoid cells (PMCs), whereas its receptor was present in LCs and in GFRA1(+) A(und). Taken together, our findings strongly suggest that LCs, different from PMCs, might play a minor role in the SSC niche and physiology and that these steroidogenic cells are probably involved in the differentiation of A(und) toward type A(1) spermatogonia.


Assuntos
Espermatogônias/metabolismo , Nicho de Células-Tronco/fisiologia , Animais , Artiodáctilos/fisiologia , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/análise , Células Intersticiais do Testículo/citologia , Células Intersticiais do Testículo/metabolismo , Fator Estimulador de Colônias de Macrófagos/biossíntese , Masculino , Receptor de Fator Estimulador de Colônias de Macrófagos/análise , Túbulos Seminíferos/citologia , Espermatogênese/fisiologia , Espermatogônias/citologia , Células-Tronco/citologia , Células-Tronco/metabolismo
2.
Am J Reprod Immunol ; 54(5): 311-20, 2005 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-16212652

RESUMO

PROBLEM: Multiparity status has been found to bring beneficial effects both to the maintenance of pregnancy and to the offspring; however, these effects have not been fully explained. We have previously reported that placentae obtained from multiparous females belonging to a syngeneic mouse crossbreeding showed an important increase in the number of placental macrophages, suggesting that they might constitute a protective subpopulation. Taking into account that macrophage-colony stimulating factor (M-CSF) and granulocyte-colony stimulating factor (G-CSF) have proved to modulate macrophage activity and that both factors and/or their receptors have been found at feto-maternal interface, in this paper we analyzed the presence of M-CSF and G-CSF in placental tissue employing the same multiparity mouse model in order to investigate the influence of parity status on local immunoregulation factors of macrophage activity. METHOD OF STUDY: Three groups of mice (CBA/J x CBA/J) were analyzed: Primiparous Young, 3.0 +/- 0.5 months old (PY); Primiparous Old, 8.5 +/- 0.5 months old (PO) and Multiparous Old, 8.5 +/- 0.5 months old, with three to four previous pregnancies (MO). The presence of M-CSF and G-CSF in placental tissue was analyzed by immunohistochemistry. Cytokeratin (CK) and vimentin (VIM) expression and PAS staining were also studied. RESULTS: The three groups showed a similar immunostaining pattern for M-CSF in the whole placental trophoblast, while the expression of G-CSF was significantly higher only in the spongy zone in the MO group. Furthermore, all the MO placentae showed 5-11 layers of cells adjacent to the decidua, where G-CSF and M-CSF were highly detected. Conversely, they constituted a thin layer in PY and PO placentae. These cells were proved to be CK(+) and VIM(-) thus demonstrating their trophoblast origin. In addition, the layers closer to the decidua were also PAS+ suggesting that they could be interstitial cells, a type of invading trophoblast. CONCLUSIONS: In our mouse model, we observed an increase in the expression of G-CSF in placental spongiotrophoblast cells in multiparous females, which have been previously proposed as progenitors of the interstitial cells. Furthermore, this is the first report that indicates that parity status increases trophoblast invasion inducing a proliferative effect of the invading cells on the maternal tissue. We suggest that M-CSF and G-CSF secreted by these invading cells could favor the recruitment of macrophages to the trophoblast and might modulate their activity inducing a switch to a protective, non-inflammatory population.


Assuntos
Fator Estimulador de Colônias de Granulócitos/biossíntese , Fator Estimulador de Colônias de Macrófagos/biossíntese , Paridade/fisiologia , Placenta/metabolismo , Gravidez/fisiologia , Animais , Feminino , Imuno-Histoquímica/métodos , Troca Materno-Fetal/fisiologia , Camundongos , Placenta/citologia
3.
s.l; s.n; Ene.-Feb 1990. 36 p. ilus.
Não convencional em Espanhol | LILACS, Sec. Est. Saúde SP, HANSEN, Hanseníase, SESSP-ILSLACERVO, Sec. Est. Saúde SP | ID: biblio-1242327

RESUMO

Se realiza una revision de la patogenia de la lepra (Hanseniasis), en sus vinculaciones con el "sistema monotitico-macrofagico" y se efectua el estudio histopatologico, histoquimico (lipidico) y con microscopia electronica de cuatro enfermos de lepra, dos lepromatosos (sin y con eritema nudoso) y otros dos dimorfos ("Borderline"). Se concluye que: 1) La lepra presenta sus manifestaciones clinico-patologicas mas ostensibles, en vinculacion con lesiones del "sistema manocitico-macrofagico". 2) Existem distintos comportamientos de los macrofagos frente al Mycobacterium leprae: a) en personas Mitsuda-positivos de puede demostrar el predominio de "macrofagos lisadores del M. leprae" con muerte y desaparicion de los bacilos; b)en individuos Mitsuda-negativos predominan los "macrofagos no-lisadores del M. leprae", que tambiem producen al muerte de los bacilos, pero con persistencia de la "envoltura lipidica bacilar", que se deposita en las vacuolas de los virchowianos: y c) en enfermos Mitsuda-negativos, luego de fromado el "granuloma virchowiano", se desarrollan los "macrofagos lisadores de las celulas de Virchow" que permitiram el recambio celular de los virchowianos. 3) los "macrofagos lisadores del M. leprae" obtienen informacion antigenica del "bacilo aislado" que puedem transmitir al sistema de inmunidad celular, cuyos linfocitos T activados generan los "granulomas epitelioides con celulas de Langhans" (granulomas tuberculoides), de la Lepra tuberculoide. 4) Los "macrofagos no-lisadores del M. leprae" no obtendrian infromacion antigenica adecuada y no tendrian capacidad para estimular ningun sistema inmunologico (celular, o humoral), originando los "granulomas virchowianos" de la lepra lepromatosa. 5) Luego del envejecimiento y muerte de los virchowianos, los "macrofagos lisadores de las celulas de Virchow" obtendrian informacion antigenica de los "bacilos degenerados asociados a lipidos y glucoproteinas citoplasmaticas", con capacidad de estimulacion del sistema inmunologico humoral cuyos linfocitos B activados generarian anticuerpos complejos: a) contra bacilos ubicados en los virchowianos en la reaccion leprosa tipo 2 (eritema nudoso leprotico); b) contra la pared de vasos en la reaccion leprosa tipo 3 (fenomeno de Lucio); y c) contra tejidos del huesped (enfermedad autoagresiva hanseniana-Azulay)


Assuntos
Humanos , Fator Estimulador de Colônias de Macrófagos , Fator Estimulador de Colônias de Macrófagos/biossíntese , Hanseníase/parasitologia , Mycobacterium leprae/citologia , Mycobacterium leprae/fisiologia , Mycobacterium leprae/genética , Mycobacterium leprae/patogenicidade
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