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The involvement of PI3K-mediated and L-VGCC-gated transient Ca2+ influx in 17β-estradiol-mediated protection of retinal cells from H2O2-induced apoptosis with Ca2+ overload.

Intracellular calcium concentration ([Ca.sup.2+ ].sub.i) plays an important role in regulating most cellular processes, including apoptosis and survival, but its alterations are different and complicated under diverse conditions. In this study, we focused on the [Ca.sup.2+ ].sub.i and its control me... Full description

Journal Title: PloS one 2013, Vol.8(11), p.e77218
Main Author: Feng, Yan
Other Authors: Wang, Baoying , Du, Fangying , Li, Hongbo , Wang, Shaolan , Hu, Chenghu , Zhu, Chunhui , Yu, Xiaorui
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0077218
Link: http://search.proquest.com/docview/1458505205/?pq-origsite=primo
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title: The involvement of PI3K-mediated and L-VGCC-gated transient Ca2+ influx in 17β-estradiol-mediated protection of retinal cells from H2O2-induced apoptosis with Ca2+ overload.
format: Article
creator:
  • Feng, Yan
  • Wang, Baoying
  • Du, Fangying
  • Li, Hongbo
  • Wang, Shaolan
  • Hu, Chenghu
  • Zhu, Chunhui
  • Yu, Xiaorui
subjects:
  • Animals–Pharmacology
  • Apoptosis–Metabolism
  • Calcium Channel Blockers–Drug Effects
  • Calcium Channels, L-Type–Pharmacology
  • Calcium Signaling–Pharmacology
  • Cell Survival–Pharmacology
  • Cells, Cultured–Pharmacology
  • Chromones–Pharmacology
  • Cytoprotection–Pharmacology
  • Estradiol–Pharmacology
  • Hydrogen Peroxide–Antagonists & Inhibitors
  • Morpholines–Metabolism
  • Neuroprotective Agents–Physiology
  • Nifedipine–Physiology
  • Oxidants–Physiology
  • Oxidative Stress–Physiology
  • Phosphatidylinositol 3-Kinases–Physiology
  • Primary Cell Culture–Physiology
  • Rats–Physiology
  • Rats, Sprague-Dawley–Physiology
  • Retinal Neurons–Physiology
  • Calcium Channel Blockers
  • Calcium Channels, L-Type
  • Chromones
  • Morpholines
  • Neuroprotective Agents
  • Oxidants
  • 2-(4-Morpholinyl)-8-Phenyl-4h-1-Benzopyran-4-One
  • Estradiol
  • Hydrogen Peroxide
  • Phosphatidylinositol 3-Kinases
  • Nifedipine
ispartof: PloS one, 2013, Vol.8(11), p.e77218
description: Intracellular calcium concentration ([Ca.sup.2+ ].sub.i) plays an important role in regulating most cellular processes, including apoptosis and survival, but its alterations are different and complicated under diverse conditions. In this study, we focused on the [Ca.sup.2+ ].sub.i and its control mechanisms in process of hydrogen peroxide (H.sub.2 O.sub.2 )-induced apoptosis of primary cultured Sprague-Dawley (SD) rat retinal cells and 17[beta]-estradiol ([beta]E2) anti-apoptosis. Fluo-3AM was used as a Ca.sup.2+ indicator to detect [Ca.sup.2+ ].sub.i through fluorescence-activated cell sorting (FACS), cell viability was assayed using MTT assay, and apoptosis was marked by Hoechst 33342 and annexin V/Propidium Iodide staining. Besides, PI3K activity was detected by Western blotting. Results showed: a) 100 [mu]M H.sub.2 O.sub.2 -induced retinal cell apoptosis occurred at 4 h after H.sub.2 O.sub.2 stress and increased in a time-dependent manner, but [Ca.sup.2+ ].sub.i increased earlier at 2 h, sustained to 12 h, and then recovered at 24 h after H.sub.2 O.sub.2 stress; b) 10 [mu]M [beta]E2 treatment for 0.5-24 hrs increased cell viability by transiently increasing [Ca.sup.2+ ].sub.i, which appeared only at 0.5 h after [beta]E2 application; c) increased [Ca.sup.2+ ].sub.i under 100 [micro]M H.sub.2 O.sub.2 treatment for 2 hrs or 10 [micro]M [beta]E2 treatment for 0.5 hrs was, at least partly, due to extracellular Ca.sup.2+ stores; d) importantly, the transiently increased [Ca.sup.2+ ].sub.i induced by 10 [micro]M [beta]E2 treatment for 0.5 hrs was mediated by the phosphatidylinositol-3-kinase (PI3K) and gated by the L-type voltage-gated Ca.sup.2+ channels (L-VGCC), but the increased [Ca.sup.2+ ].sub.i induced by 100 [micro]M H.sub.2 O.sub.2 treatment for 2 hrs was not affected; and e) pretreatment with 10 [micro]M [beta]E2 for 0.5 hrs effectively protected retinal cells from apoptosis induced by 100 [micro]M H.sub.2 O.sub.2, which was also associated with its transient [Ca.sup.2+ ].sub.i increase through L-VGCC and PI3K pathway. These findings will lead to better understanding of the mechanisms of [beta]E2-mediated retinal protection and to exploration of the novel therapeutic strategies for retina degeneration.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0077218
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleThe involvement of PI3K-mediated and L-VGCC-gated transient Ca2+ influx in 17β-estradiol-mediated protection of retinal cells from H2O2-induced apoptosis with Ca2+ overload.
creatorFeng, Yan ; Wang, Baoying ; Du, Fangying ; Li, Hongbo ; Wang, Shaolan ; Hu, Chenghu ; Zhu, Chunhui ; Yu, Xiaorui
contributorFeng, Yan (correspondence author) ; Feng, Yan (record owner)
ispartofPloS one, 2013, Vol.8(11), p.e77218
identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0077218
subjectAnimals–Pharmacology ; Apoptosis–Metabolism ; Calcium Channel Blockers–Drug Effects ; Calcium Channels, L-Type–Pharmacology ; Calcium Signaling–Pharmacology ; Cell Survival–Pharmacology ; Cells, Cultured–Pharmacology ; Chromones–Pharmacology ; Cytoprotection–Pharmacology ; Estradiol–Pharmacology ; Hydrogen Peroxide–Antagonists & Inhibitors ; Morpholines–Metabolism ; Neuroprotective Agents–Physiology ; Nifedipine–Physiology ; Oxidants–Physiology ; Oxidative Stress–Physiology ; Phosphatidylinositol 3-Kinases–Physiology ; Primary Cell Culture–Physiology ; Rats–Physiology ; Rats, Sprague-Dawley–Physiology ; Retinal Neurons–Physiology ; Calcium Channel Blockers ; Calcium Channels, L-Type ; Chromones ; Morpholines ; Neuroprotective Agents ; Oxidants ; 2-(4-Morpholinyl)-8-Phenyl-4h-1-Benzopyran-4-One ; Estradiol ; Hydrogen Peroxide ; Phosphatidylinositol 3-Kinases ; Nifedipine
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descriptionIntracellular calcium concentration ([Ca.sup.2+ ].sub.i) plays an important role in regulating most cellular processes, including apoptosis and survival, but its alterations are different and complicated under diverse conditions. In this study, we focused on the [Ca.sup.2+ ].sub.i and its control mechanisms in process of hydrogen peroxide (H.sub.2 O.sub.2 )-induced apoptosis of primary cultured Sprague-Dawley (SD) rat retinal cells and 17[beta]-estradiol ([beta]E2) anti-apoptosis. Fluo-3AM was used as a Ca.sup.2+ indicator to detect [Ca.sup.2+ ].sub.i through fluorescence-activated cell sorting (FACS), cell viability was assayed using MTT assay, and apoptosis was marked by Hoechst 33342 and annexin V/Propidium Iodide staining. Besides, PI3K activity was detected by Western blotting. Results showed: a) 100 [mu]M H.sub.2 O.sub.2 -induced retinal cell apoptosis occurred at 4 h after H.sub.2 O.sub.2 stress and increased in a time-dependent manner, but [Ca.sup.2+ ].sub.i increased earlier at 2 h, sustained to 12 h, and then recovered at 24 h after H.sub.2 O.sub.2 stress; b) 10 [mu]M [beta]E2 treatment for 0.5-24 hrs increased cell viability by transiently increasing [Ca.sup.2+ ].sub.i, which appeared only at 0.5 h after [beta]E2 application; c) increased [Ca.sup.2+ ].sub.i under 100 [micro]M H.sub.2 O.sub.2 treatment for 2 hrs or 10 [micro]M [beta]E2 treatment for 0.5 hrs was, at least partly, due to extracellular Ca.sup.2+ stores; d) importantly, the transiently increased [Ca.sup.2+ ].sub.i induced by 10 [micro]M [beta]E2 treatment for 0.5 hrs was mediated by the phosphatidylinositol-3-kinase (PI3K) and gated by the L-type voltage-gated Ca.sup.2+ channels (L-VGCC), but the increased [Ca.sup.2+ ].sub.i induced by 100 [micro]M H.sub.2 O.sub.2 treatment for 2 hrs was not affected; and e) pretreatment with 10 [micro]M [beta]E2 for 0.5 hrs effectively protected retinal cells from apoptosis induced by 100 [micro]M H.sub.2 O.sub.2, which was also associated with its transient [Ca.sup.2+ ].sub.i increase through L-VGCC and PI3K pathway. These findings will lead to better understanding of the mechanisms of [beta]E2-mediated retinal protection and to exploration of the novel therapeutic strategies for retina degeneration.
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titleThe involvement of PI3K-mediated and L-VGCC-gated transient Ca2+ influx in 17β-estradiol-mediated protection of retinal cells from H2O2-induced apoptosis with Ca2+ overload.
authorFeng, Yan ; Wang, Baoying ; Du, Fangying ; Li, Hongbo ; Wang, Shaolan ; Hu, Chenghu ; Zhu, Chunhui ; Yu, Xiaorui
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