scholarly journals Regional Expression of c-Fos and Heat Shock Protein-70 mRNA following Hypoxia-Ischemia in Immature Rat Brain

1992 ◽  
Vol 12 (6) ◽  
pp. 987-995 ◽  
Author(s):  
Ken S. Blumenfeld ◽  
Frank A. Welsh ◽  
Valerie A. Harris ◽  
Michael A. Pesenson

Cerebral ischemia induces the expression of a number of proteins that may have an important influence on cellular injury. The purpose of this study was to compare the regional effects of hypoxia–ischemia on the expression of the proto-oncogene, c-fos, and the heat shock protein-70 (HSP-70) gene in developing brain. Unilateral hypoxia–ischemia was produced in the brain of immature rats (7, 15, and 23 days after birth) using a combination of carotid artery ligation and systemic hypoxia (8% O2). After recovery for 2 and 24 h, the regional expression of c-fos and HSP-70 mRNA was determined using in situ hybridization. Littermates were permitted to recover for 1 week for assessment of histologic injury. Hypoxia–ischemia increased the expression of both c-fos and HSP-70 mRNA, but the topography of expression varied with the age of the animal as well as the mRNA species. In the 7-day-old group, expression of c-fos at 2 h increased in multiple regions of the ipsilateral hemisphere in nearly one-half of the animals, while HSP-70 mRNA was not expressed until 24 h and, then, predominantly in the hippocampus. In 15- and 23-day-old rats, expression of c-fos was increased at 2 h in the entorhinal cortex and in the dendritic field of the upper blade of the hippocampal dentate gyrus, while HSP-70 mRNA was prominently expressed in neocortex and the cell layers of the hippocampus. Interestingly, the strong expression of HSP-70 mRNA in dentate granule cells did not occur in the innermost layer of cells. By 24 h of recovery, expression of c-fos had nearly normalized in all age groups, while HSP-70 mRNA was expressed in 15- and 23-day-old rats in many regions, including those undergoing histologic injury. These results suggest that expression of c-fos and HSP-70 mRNA may be useful regional markers of cell stress following hypoxia–ischemia.

2004 ◽  
Vol 82 (6) ◽  
pp. 363-371 ◽  
Author(s):  
R M Narayansingh ◽  
M Senchyna ◽  
M M Vijayan ◽  
J C Carlson

In this study we examined the mechanism of corpus luteum (CL) regression by measuring changes in expression of prostaglandin G/H synthase-1 (PGHS-1) and -2 (PGHS-2) in day 4 CL and inducible heat shock protein 70 (HSP-70) in day 4 and day 9 CL of immature superovulated rats. The rats were superovulated and treated with 500 µg of prostaglandin F2α (PGF2α) on day 4 or day 9 after CL formation. Ovaries and serial blood samples were removed during the 24-hour period following treatment. Plasma progesterone was determined by radioimmunoassay while mRNA abundance and protein expression were assessed by semiquantitative RT-PCR and immunoblot analysis, respectively. One hour after PGF2α, both day 4 and day 9 rats exhibited a significant decrease in progesterone secretion; however, there was a greater decrease in day 9 rats. In ovarian samples removed on day 4, there was a significant increase in mRNA for PGHS-2 at 1 hour after PGF2α. PGHS-1 mRNA content remained unchanged. Immunoblot analyses showed an increase in PGHS-2 protein expression only at 8 h. There were no changes in PGHS-1 protein expression. In day 9 rats, ovarian HSP-70 protein levels increased by 50% after PGF2α injection; however, on day 4 there was no change in expression of this protein over the sampling period. These results suggest that expression of PGHS-2 may be involved in inhibiting progesterone production and that expression of HSP-70 may be required for complete CL regression in the rat.Key words: rat, prostaglandin F2α, corpus luteum, prostaglandin G/H synthase, heat shock protein-70.


2014 ◽  
Author(s):  
Δημήτριος Λυσίτσας

Εισαγωγή: Η υπερπλασία του έσω χιτώνα παίζει μείζων ρόλο στην επαναστένωση (in-stentrestenosis). Στην παρούσα μελέτη αξιολογήσαμε in vitro την επίδραση της D-24851(κυτταροτοξική ουσία που σταματά τον κυτταρικό κύκλο στο στάδιο G2-M) στονπολλαπλασιασμό των λείων μυϊκών κυττάρων και μελετήσαμε την ασφάλεια και τηνδραστικότητα μίας ενδαγγειακής πρόθεσης (stent) επικαλυμμένης με πολυμερή ουσία πουαπελευθερώνει την D-24851, στην αναστολή της υπερπλασίας του έσω χιτώνα χωρίς ναεμποδίζει την αναγεννητική ικανότητα του ενδοθηλίου σε in vivo πειραματικό μοντέλο.Υλικό και Μέθοδοι: Γυμνά μεταλλικά stent (n=6), stent επικαλυμμένα μόνο με πολυμερήουσία (polymer-coated, n=7) και stent επικαλυμμένα με πολυμερή ουσία πουαπελευθερώνουν 31±1μg (low-dose, n=7), 216±8 μg (high-dose, n=6) ή 1774±39 μg(extreme-dose, n=5) της D-24851 εμφυτεύτηκαν στις μηριαίες αρτηρίες λευκών New Zealandκουνελιών. Τα πειραματόζωα θυσιάστηκαν στις 28 ημέρες για ιστομορφομετρική ανάλυση.Για την αξιολόγηση της ενδοθηλιακής αναγέννησης στις 90 ημέρες, 12 πειραματόζωαχρησιμοποιήθηκαν για την τοποθέτηση polymer-coated (n=3), low dose (n=3), high dose(n=3) or extreme dose (n=3) ενδαγγειακών προθέσεων.Αποτελέσματα: In vitro η D-24851 αναστέλλει την υπερπλασία των λείων μυϊκών κυττάρωνκαι επάγει την απόπτωση τους χωρίς να αυξάνει την επαγωγή της heat shock protein 70(HSP-70), μία κυτταροπροστατευτική και αντι-αποπτωτική πρωτεΐνη. Η θεραπεία με lowdoseD-24851 stents συνδυάστηκε με 38% (P=0.029) μείωση της υπερπλαστικής περιοχήςτου έσω χιτώνα και 35% (P=0.003) μείωση της επι τοις εκατό στένωσης του αυλού σεσύγκριση με τα γυμνά μεταλλικά stents. Ο τραυματισμός και η φλεγμονή του αρτηριακού τοιχώματος δεν παρουσίασαν σημαντικές διαφορές μεταξύ των ομάδων. Τα επικαλυμμέναμόνο με πολυμερή ουσία stents εμφάνισαν παρόμοια ανάπτυξη νεοιστού σε σύγκριση με ταγυμνά μεταλλικά stents. Ωστόσο, όλες οι ομάδες των stents με D-24851 παρουσίασαν ατελήενδοθηλιοποίηση συγκρινόμενα με τα polymer-coated stents.Συμπεράσματα: Οι επικεκαλυμμένες ενδαγγειακές προσθέσεις με πολυμερή ουσία καιχαμηλη δόση D-24851 μειώνουν σημαντικά την υπερπλασιά του έσω χιτώνα. Λόγω τηςατελούς ενδοθηλιοποίησης, μακράς διάρκειας μελέτες είναι απαραίτητες για ναπιστοποιήσουν ότι η αναστολή του νεοιστού παραμένει και μετά τις 28 ημέρες.


Biomedika ◽  
2015 ◽  
Vol 7 (2) ◽  
Author(s):  
Mochammad Arief Taufiqurochman

Penelitian dilakukan untuk mengetahui efek paparan medan elektromagnetik ELF sebesar 100 μT 8 jam/ hari selama 2 dan 4 minggu terhadap ekspresi HSP 70 makrofag peritoneum mencit yang diinfeksi dengan Toxoplasma gondii. Jenis penelitian ini adalah Eksperimen Biomedik menggunakan rancangan randomized separate posttest control group designdengan hewan coba mencit strain Balb/c, melalui pengamatan ekspresi HSP 70 , terdiri dari 3 kelompok kontrol dan 4 kelompok perlakuan, tiap kelompok terdiri dari 4 hewan coba. Pengamatan jaringan menggunakan metode imunohistokimia indirek, hasilnya dianalisis menggunakan uji statistik Independent t-test antar kelompok setelah dilakukan uji homogenitas dan normalitas data penelitian ( α=0.05). Hasil penelitian menunjukkan bahwa akibat paparanME ELF dengan itensitas 100 μT selama 2 minggu belum mampu melemahkan atau memutus rantai DNA gen HSP 70 promotor region tetapi menimbulkan stres seluler yang berakibat teraktifasinya HSF 1 melalui konversi menjadi trimer yang akan meregulasi secara cepat sintesis HSP 70 . Paparan medan elektromegnetik ME ELF selama 4 minggu dapat melemahkan bahkan memutus rantai DNA hsp 70 promotor region, sehingga sintesis HSP akan terhambat secara signifikan (p<0.05). Terdapat peningkatan secara signifikan ekspresi HSP 70 makrofag peritoneum mencit yang terpapar ME ELF dengan itensitas 100 μT selama 2 minggu pada kelompok yang terinfeksi toxoplasma gondii dan terjadi penurunan secara signifikan ekspresi HSP 70 pada kelompok terpapar ME ELF selama4 minggu pada kelompok yang terinfeksi Toxoplasma gondi dibandingkan dengan konrol.Kata Kunci: Medan Electromagnetik ELF, HSP 70, Makrofag, Toxoplasma gondii.


1995 ◽  
Vol 15 (6) ◽  
pp. 1047-1056 ◽  
Author(s):  
Shuichi Kobayashi ◽  
Frank A. Welsh

Neonatal rats, 7 days of age, underwent unilateral carotid artery ligation followed by exposure to hypoxia (8% O2) for 80 min. At the end of the period of hypoxia, and after recovery for 2 or 24 h, regional levels of ATP and heat-shock protein-72 (hsp72) mRNA were measured in adjacent brain sections using ATP-luminescence histochemistry and in situ hybridization, respectively. At the end of hypoxia, ATP levels were decreased in a patchy pattern within the hemisphere ipsilateral to the carotid ligation. In the parietal cortex, the reduction of ATP often occurred in columns oriented perpendicular to the cortical surface. Expression of hsp72 mRNA was not detected prior to recovery, except in the ventricular lining of the ipsilateral hemisphere. However, by 2 h of recovery, hsp72 mRNA was expressed in a diffuse pattern in the ipsilateral hemisphere, even in regions in which the distribution of ATP remained patchy. Although the regional extent of expression varied in different animals, hsp72 mRNA was expressed consistently in the subcortical white matter, which, in some animals, was the only region showing expression. In contrast to the diffuse pattern of expression at 2 h of recovery, expression of hsp72 mRNA at 24 h was highly localized in the superficial layers of cerebral cortex and the pyramidal cell layer of hippocampus. The present results demonstrate that hypoxia–ischemia causes regionally distinct alterations in ATP and hsp72 mRNA that may be related to cell injury in this model.


2005 ◽  
Vol 60 (8) ◽  
pp. 963-969 ◽  
Author(s):  
J. W. Starnes ◽  
A. M. Choilawala ◽  
R. P. Taylor ◽  
M. J. Nelson ◽  
M. D. Delp

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