Browsing by Author "Chacon, Cecilia"

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    Expression and immunolocalization of endothelin peptides and its receptors, ETA and ETB, in the carotid body exposed to chronic intermittent hypoxia
    (2007) Rey, Sergio; Corthorn, Jenny; Chacon, Cecilia; Iturriaga, Rodrigo
    Increased levels of endothelin-1 (ET-1) in the carotid body (CB) contribute to the enhancement of chemosensory responses to acute hypoxia in cats exposed to chronic intermittent hypoxia (CIH). However, it is not known if the ET receptor types A (ETA-R) and B (ETB-R) are upregulated. Thus, we studied the expression and localization of ETA-R and ETB-R using Western blot and immunohistochemistry (IHC) in CBs from cats exposed to cyclic hypoxic episodes, repeated during 8 hr for 4 days. In addition, we determined if ET-1 is expressed in the chemoreceptor cells using double immunofluorescence for ET-1 ancityrosine hydroxylase (TH). We found that ET-1 expression was ubiquitous in the blood vessels and CB parenchyma, although double ET-1 and TH-positive chemoreceptor cells were mostly found in the parenchyma. ETA-R was expressed in most chemoreceptor cells and blood vessels of the CB vascular pole. ETB-R was expressed in chemoreceptor cells, parenchymal capillaries, and blood vessels of the vascular pole. CIH upregulated ETB-R expression by similar to 2.1 (Western blot) and 1.6-fold (IHC) but did not change ETA-R expression. Present results suggest that ET-1, ETA-R, and ETB-R are involved in the enhanced CB chemosensory responses to acute hypoxia induced by CIH.
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    Expression of gremlin, a bone morphogenetic protein antagonist, is associated with vascular calcification in uraemia
    (OXFORD UNIV PRESS, 2009) Jara, Aquiles; Chacon, Cecilia; Eugenia Burgos, Maria; Droguett, Alejandra; Valdivieso, Andres; Ortiz, Mireya; Troncoso, Pablo; Mezzano, Sergio
    Background. Vascular calcification has been widely recognized as a significant contributor to cardiovascular risk in patients with chronic kidney disease. Recent evidence suggests that BMP-7 decreases the vascular calcification observed in uraemic rats, while BMP-2 could also be participating in this process. Gremlin, a bone morphogenetic protein antagonist, has been detected in rat aortic vascular smooth muscle cells (VSMCs), and since the role of the VSMCs into vascular calcification in uraemia is considered critical in this process, we hypothesized that gremlin could be participating in its pathogenesis. With this aim, we studied its expression in aorta from uraemic rats with calcitriol-induced vascular calcification and in 16-vessel biopsies of uraemic patients undergoing kidney transplantation.
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    Expression of kallikrein, bradykinin B2 receptor, and endothelial nitric oxide synthase in placenta in normal gestation, preeclampsia, and placenta accreta
    (2006) Corthorn, Jenny; Germain, Alfredo A.; Chacon, Cecilia; Rey, Sergio; Soto, Gloria X.; Figueroa, Carlos D.; Mueller-Esterl, Werner; Duarte, Ignacio; Valdes, Gloria
    In an effort to define the varied expression of three vasoactive markers in the clinical models of normal placenta/normal invasion (n = 11), preeclampsia/restricted trophoblast invasion (n = 15), and placenta accreta/exaggerated invasion (n = 6), we performed semiquantitative immunohistochemistry for kallikrein, bradykinin 132 receptor, and endothelial nitric oxide synthase (eNOS). In the floating villi, the syncytiotrophoblast expressed more kallikrein in placenta accreta (p < 0.05), than in normal and preeclamptic placentas, while the bradykinin B2 receptor and eNOS were similarly expressed in all groups; in the fetal endothelium, the bradykinin B2 receptor was enhanced in placenta accreta (p < 0.005), but kallikrein and eNOS were similarly expressed in the other two groups. in the extravillous trophoblast, both kallikrein and eNOS expression were higher in placenta accreta (p < 0.001), while the bradykinin B2 receptor signal was only enhanced in preeclampsia (p < 0.05). The presence and localization of kallikrein, the bradykinin B2 receptor, and eNOS in the fetomaternal interface in the three study conditions supports a local role for interrelated vasodilatory/antiaggregating systems. This first report of the variations observed in kallikrein and eNOS in a condition of exaggerated trophoblast invasion supports the participation of vasodilatation in trophoblast migration.