scholarly journals U0126 Attenuates Cerebral Vasoconstriction and Improves Long-Term Neurologic Outcome after Stroke in Female Rats

2015 ◽  
Vol 35 (3) ◽  
pp. 454-460 ◽  
Author(s):  
Hilda Ahnstedt ◽  
Maryam Mostajeran ◽  
Frank W Blixt ◽  
Karin Warfvinge ◽  
Saema Ansar ◽  
...  
Keyword(s):  
Organ Culture ◽  
Infarct Size ◽  
Cerebral Arteries ◽  
Female Rats ◽  
Experimental Stroke ◽  
In Vitro Organ Culture ◽  
Neurologic Function ◽  
Receptor Upregulation

Sex differences are well known in cerebral ischemia and may impact the effect of stroke treatments. In male rats, the MEK1/2 inhibitor U0126 reduces ischemia-induced endothelin type B (ETB) receptor upregulation, infarct size and improves acute neurologic function after experimental stroke. However, responses to this treatment in females and long-term effects on outcome are not known. Initial experiments used in vitro organ culture of cerebral arteries, confirming ERK1/2 activation and increased ETB receptor-mediated vasoconstriction in female cerebral arteries. Transient middle cerebral artery occlusion (tMCAO, 120 minutes) was induced in female Wistar rats, with U0126 (30 mg/kg intraperitoneally) or vehicle administered at 0 and 24 hours of reperfusion, or with no treatment. Infarct volumes were determined and neurologic function was assessed by 6-point and 28-point neuroscores. ETB receptor-mediated contraction was studied with myograph and protein expression with immunohistochemistry. In vitro organ culture and tMCAO resulted in vascular ETB receptor upregulation and activation of ERK1/2 that was prevented by U0126. Although no effect on infarct size, U0126 improved the long-term neurologic function after experimental stroke in female rats. In conclusion, early prevention of the ERK1/2 activation and ETB receptor-mediated vasoconstriction in the cerebral vasculature after ischemic stroke in female rats improves the long-term neurologic outcome.

In vivo experimental stroke and in vitro organ culture induce similar changes in vasoconstrictor receptors and intracellular calcium handling in rat cerebral arteries

2012 ◽  
Vol 219 (4) ◽  
pp. 507-520 ◽  
Author(s):  
Gro Klitgaard Povlsen ◽  
Roya Waldsee ◽  
Hilda Ahnstedt ◽  
Kim Anker Kristiansen ◽  
Flemming Fryd Johansen ◽  
...  
Keyword(s):  
Organ Culture ◽  
Intracellular Calcium ◽  
Cerebral Arteries ◽  
Calcium Handling ◽  
Experimental Stroke ◽  
In Vitro Organ Culture

The Influence of Fluoride Exposure on Dentin Mineralization Using an in Vitro Organ Culture Model

2003 ◽  
Vol 73 (5) ◽  
pp. 470-475 ◽  
Author(s):  
R. Moseley ◽  
R. J. Waddington ◽  
A. J. Sloan ◽  
A. J. Smith ◽  
R. C. Hall ◽  
...  
Keyword(s):  
Organ Culture ◽  
Fluoride Exposure ◽  
Culture Model ◽  
Dentin Mineralization ◽  
In Vitro Organ Culture

Development of an in vitro organ culture model to study transmission of HIV-1 in the female genital tract

10.1038/74743 ◽  
2000 ◽  
Vol 6 (4) ◽  
pp. 475-479 ◽  
Author(s):  
Kelly B. Collins ◽  
Bruce K. Patterson ◽  
Gregory J. Naus ◽  
Daniel V. Landers ◽  
Phalguni Gupta
Keyword(s):  
Organ Culture ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Culture Model ◽  
In Vitro Organ Culture ◽  
Hiv 1 ◽  
Female Genital

scholarly journals Adherence of enteroaggregative Escherichia coli to the ileal and colonic mucosa: an in vitro study utilizing the scanning electron microscopy

2011 ◽  
Vol 48 (3) ◽  
pp. 199-204 ◽  
Author(s):  
Jacy Alves Braga de Andrade ◽  
Edna Freymüller ◽  
Ulysses Fagundes-Neto
Keyword(s):  
Escherichia Coli ◽  
Organ Culture ◽  
Colonic Mucosa ◽  
In Vitro Study ◽  
In Vitro Assays ◽  
Electron Microscopic ◽  
In Vitro Organ Culture ◽  
Scanning Electron

CONTEXT: Enteroaggregative Escherichia coli strains have been associated with persistent diarrhea in several developing countries. In vivo procedures with animal models, in vitro assays with cellular lines and in vitro organ culture with intestinal fragments have been utilized to study these bacteria and their pathogenicity. OBJECTIVE: The present experimental research assessed the pathogenic interactions of three enteroaggregative Escherichia coli strains, using the in vitro organ culture, in order to show the adherence to different regions of both, the ileal and the colonic mucosa and demonstrate possible mechanisms that could have the participation in the prolongation of diarrheiogenic process. METHODS: This study used intestinal fragments from terminal ileum and colon that were excised from pediatric patients undergoing intestinal surgeries and from adult patients that underwent to colonoscopic procedures. Each strain was tested with three intestinal fragments for each region. Tissue was fixed for scanning electron microscopic analysis. RESULTS: These bacteria colonized ileal and colonic mucosa in the typical stacked-brick configuration in the ileum and colon. In both regions, the strains were seen over a great amount of mucus and sometimes over the intact epithelium. In some regions, there is a probable evidence of effacement of the microvilli. It was possible to see adhered to the intestinal surface, bacteria fimbrial structures that could be responsible for the adherence process. CONCLUSION: In order to cause diarrhea, enteroaggregative Escherichia coli strains adhere to the intestinal mucosa, create a mucoid biofilm on the small bowel surface that could justify the digestive-absorptive abnormalities and consequently, prolonging the diarrhea.

Abstract 15884: Cardiosphere-Derived Cells Confer Acute Cardioprotection Following Ischemia-Reperfusion Injury in Rats: Role of Macrophage Polarization

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Geoffrey de Couto ◽  
Hideaki Kanazawa ◽  
Eleni Tseliou ◽  
Linda Marbán ◽  
Eduardo Marbán
Keyword(s):  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Macrophage Polarization ◽  
Oxidant Stress ◽  
Gene Profiles ◽  
Wistar Kyoto ◽  
Inflammatory Response To Injury

Introduction: Cardiosphere-derived cells (CDCs) confer both cardioprotection and regeneration in acute myocardial infarction (MI). However, only long-term (>3 wks) post-MI endpoints have been studied, making it impossible to investigate the cardioprotective effects in isolation. Macrophages (MF) concentrate within the heart following ischemic injury as part of the inflammatory response to injury. Here we test the hypothesis that CDCs are cardioprotective by modifying MF within the myocardium post-MI. Methods & Results: Wistar-Kyoto rats (aged 8-12 wks) underwent 45 min of ischemia followed by 20 min of reperfusion, then intracoronary (i.c.) infusion of either saline or CDCs (5x10 5 ). The use of a 48 hr endpoint enabled the selective study of cardioprotection. CDC-treated animals had preserved ejection fraction (59.2% vs. 47.4%; p<0.001) and reduced infarct size (TTC; 6.3% vs. 13.6%; p<0.01). The finding that CDC-treated hearts contained fewer CD68 + MF (p<0.05) suggested a mechanistic role for MF, a conjecture which we tested in detail. MF isolated from CDC-treated hearts secreted lower amounts of proinflammatory cytokines ( Nos2, Tnf, Il1b ; p<0.05). Systemic depletion of MF with clodronate liposomes attenuated the benefits of CDC therapy post-MI (p<0.05). In vitro , MF conditioned by transwell exposure to CDCs (M CDC ) exhibited distinct gene profiles relative to proinflammatory M 1 or “healing” M 2 polarization states (M CDC : Il10 ; M 1 : Nos2 ; M 2 : Arg1, Pparg ). Adoptive transfer of selective MF populations into the heart (i.c.; 20 min post-reflow) revealed that M CDC , but not M 1 or M 2 MF, could recapitulate the reduction in infarct size (M CDC : 4.5%; M 1 : 14.0%; M 2 : 10.8%; p<0.05). In vitro co-culture shows that M CDC selectively reduce cardiomyocyte apoptosis following oxidant stress (M CDC : 9.9%; M 1 : 39.4%; M 2 : 37.4%; p<0.001). Conclusions: CDCs are cardioprotective when administered 20 min after reflow; the timing distinguishes this form of cardioprotection from preconditioning or ischemic postconditioning. Various lines of evidence indicate that CDCs work by polarizing MF toward a cardioprotective phenotype. The findings motivate further translational development of the adjunctive use of CDCs post-MI to limit infarct size.

Growth hormone and somatostatin directly inhibit gastric ghrelin secretion. An in vitro organ culture system

2007 ◽  
Vol 30 (9) ◽  
pp. RC22-RC25 ◽  
Author(s):  
L. M. Seoane ◽  
O. Al-Massadi ◽  
F. Barreiro ◽  
C. Dieguez ◽  
F.F Casanueva
Keyword(s):  
Growth Hormone ◽  
Organ Culture ◽  
Culture System ◽  
Organ Culture System ◽  
In Vitro Organ Culture ◽  
Ghrelin Secretion
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