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פותח על ידי קלירמאש פתרונות בע"מ -
Manipulations of ACHE gene expression suggest non-catalytic involvement of acetylcholinesterase in the functioning of mammalian photoreceptors but not in retinal degeneration
Year:
1999
Source of publication :
Molecular Brain Research
Authors :
שני, משה
;
.
Volume :
71
Co-Authors:
Broide, R.S., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel, Baylor College of Medicine, Houston, TX 77030, United States
Grifman, M., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Loewenstein, A., Department of Ophthalmology, Surasky Medical Center, 64329, Tel Aviv, Israel
Grisaru, D., Dept. of Obstetrics and Gynecology, Surasky Medical Center, 64329, Tel Aviv, Israel
Timberg, R., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Stone, J., New S. Wales Retinal Dystrophy R., Sydney University, Sydney, NSW 2006, Australia
Shani, M., Institute of Animal Science, Volcani Center, Bet Dagan, 50250, Israel
Patrick, J.W., Baylor College of Medicine, Houston, TX 77030, United States
Soreq, H., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Facilitators :
From page:
137
To page:
148
(
Total pages:
12
)
Abstract:
To explore role(s) of acetylcholinesterase (AChE) in functioning and diseased photoreceptors, we studied normal (rd/+) and degenerating (rd/rd) murine retinas. All retinal neurons, expressed AChEmRNA throughout fetal development. AChE and c-Fos mRNAs peaked at post-natal days 10-12, when apoptosis of rd/rd photoreceptors begins. Moreover, c-Fos and AChEmRNA were co-overexpressed in rd/rd mice producing transgenic human (h), and host (m) AChE, but not in rd/+ mice. However, mAChE overexpression also occurred in transgenics expressing human serum albumin. Drastic variations in AChE catalytic activity were ineffective during development. Neither transgenic excess nor diisopropylfluorophosphonate (DFP) inhibition (80%) affected the rd phenotype; nor did DFP exposure induce photoreceptor degeneration or affect other key cholinergic proteins in rd/+ mice, unlike reports of adult mice and despite massive induction under DFP of c-Fos overproduction. In human embryos (20 weeks), most retinal neurons express AChEmRNA. Surprisingly, only the continually remodeling photoreceptors express AChEmRNA in aged humans (> 70 years). Therefore, the extreme retinal sensitivity to AChE modulation may reflect non-catalytic function(s) of AChE in adult photoreceptors. These findings exclude AChE as causing the rd phenotype, suggest that its primary function(s) in mammalian retinal development are non-catalytic ones and indicate special role(s) for the AChE protein in adult photoreceptors.
Note:
Related Files :
Acetylcholinesterase
adult
Animals
animal tissue
apoptosis
gene expression
Mammalia
mice
phenotype
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/S0169-328X(99)00169-2
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
23503
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:00
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Scientific Publication
Manipulations of ACHE gene expression suggest non-catalytic involvement of acetylcholinesterase in the functioning of mammalian photoreceptors but not in retinal degeneration
71
Broide, R.S., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel, Baylor College of Medicine, Houston, TX 77030, United States
Grifman, M., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Loewenstein, A., Department of Ophthalmology, Surasky Medical Center, 64329, Tel Aviv, Israel
Grisaru, D., Dept. of Obstetrics and Gynecology, Surasky Medical Center, 64329, Tel Aviv, Israel
Timberg, R., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Stone, J., New S. Wales Retinal Dystrophy R., Sydney University, Sydney, NSW 2006, Australia
Shani, M., Institute of Animal Science, Volcani Center, Bet Dagan, 50250, Israel
Patrick, J.W., Baylor College of Medicine, Houston, TX 77030, United States
Soreq, H., Department of Biological Chemistry, Inst. Life Sci., Hebrew Univ. J., Jerusalem, Israel
Manipulations of ACHE gene expression suggest non-catalytic involvement of acetylcholinesterase in the functioning of mammalian photoreceptors but not in retinal degeneration
To explore role(s) of acetylcholinesterase (AChE) in functioning and diseased photoreceptors, we studied normal (rd/+) and degenerating (rd/rd) murine retinas. All retinal neurons, expressed AChEmRNA throughout fetal development. AChE and c-Fos mRNAs peaked at post-natal days 10-12, when apoptosis of rd/rd photoreceptors begins. Moreover, c-Fos and AChEmRNA were co-overexpressed in rd/rd mice producing transgenic human (h), and host (m) AChE, but not in rd/+ mice. However, mAChE overexpression also occurred in transgenics expressing human serum albumin. Drastic variations in AChE catalytic activity were ineffective during development. Neither transgenic excess nor diisopropylfluorophosphonate (DFP) inhibition (80%) affected the rd phenotype; nor did DFP exposure induce photoreceptor degeneration or affect other key cholinergic proteins in rd/+ mice, unlike reports of adult mice and despite massive induction under DFP of c-Fos overproduction. In human embryos (20 weeks), most retinal neurons express AChEmRNA. Surprisingly, only the continually remodeling photoreceptors express AChEmRNA in aged humans (> 70 years). Therefore, the extreme retinal sensitivity to AChE modulation may reflect non-catalytic function(s) of AChE in adult photoreceptors. These findings exclude AChE as causing the rd phenotype, suggest that its primary function(s) in mammalian retinal development are non-catalytic ones and indicate special role(s) for the AChE protein in adult photoreceptors.
Scientific Publication
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