Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Erythropoietin Signaling Increases Choroidal Macrophages and Cytokine Expression, and Exacerbates Choroidal Neovascularization

CA. Bretz, V. Divoky, J. Prchal, E. Kunz, AB. Simmons, H. Wang, ME. Hartnett,

. 2018 ; 8 (1) : 2161. [pub] 20180201

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc19000947

Erythropoietin (EPO) is recognized for neuroprotective and angiogenic effects and has been associated with aging and neovascular age-related macular degeneration (AMD). We hypothesized that systemic EPO facilitates the development of choroidal neovascularization (CNV). Wild type mice expressed murine EPOR (mWtEPOR) in RPE/choroids at baseline and had significantly increased serum EPO after laser treatment. To test the role of EPO signaling, we used human EPOR knock-in mice with the mWtEPOR gene replaced by either the human EPOR gene (hWtEPOR) or a mutated human EPOR gene (hMtEPOR) in a laser-induced choroidal neovascularization (LCNV) model. Loss-of-function hWtEPOR mice have reduced downstream activation, whereas gain-of-function hMtEPOR mice have increased EPOR signaling. Compared to littermate controls (mWtEPOR), hMtEPOR with increased EPOR signaling developed larger CNV lesions. At baseline, hMtEPOR mice had increased numbers of macrophages, greater expression of macrophage markers F4/80 and CD206, and following laser injury, had greater expression of cytokines CCL2, CXCL10, CCL22, IL-6, and IL-10 than mWtEPOR controls. These data support a hypothesis that injury from age- and AMD-related changes in the RPE/choroid leads to choroidal neovascularization through EPOR-mediated cytokine production.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc19000947
003      
CZ-PrNML
005      
20220512082047.0
007      
ta
008      
190107s2018 enk f 000 0|eng||
009      
AR
024    7_
$a 10.1038/s41598-018-20520-z $2 doi
035    __
$a (PubMed)29391474
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Bretz, Colin A $u John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA.
245    10
$a Erythropoietin Signaling Increases Choroidal Macrophages and Cytokine Expression, and Exacerbates Choroidal Neovascularization / $c CA. Bretz, V. Divoky, J. Prchal, E. Kunz, AB. Simmons, H. Wang, ME. Hartnett,
520    9_
$a Erythropoietin (EPO) is recognized for neuroprotective and angiogenic effects and has been associated with aging and neovascular age-related macular degeneration (AMD). We hypothesized that systemic EPO facilitates the development of choroidal neovascularization (CNV). Wild type mice expressed murine EPOR (mWtEPOR) in RPE/choroids at baseline and had significantly increased serum EPO after laser treatment. To test the role of EPO signaling, we used human EPOR knock-in mice with the mWtEPOR gene replaced by either the human EPOR gene (hWtEPOR) or a mutated human EPOR gene (hMtEPOR) in a laser-induced choroidal neovascularization (LCNV) model. Loss-of-function hWtEPOR mice have reduced downstream activation, whereas gain-of-function hMtEPOR mice have increased EPOR signaling. Compared to littermate controls (mWtEPOR), hMtEPOR with increased EPOR signaling developed larger CNV lesions. At baseline, hMtEPOR mice had increased numbers of macrophages, greater expression of macrophage markers F4/80 and CD206, and following laser injury, had greater expression of cytokines CCL2, CXCL10, CCL22, IL-6, and IL-10 than mWtEPOR controls. These data support a hypothesis that injury from age- and AMD-related changes in the RPE/choroid leads to choroidal neovascularization through EPOR-mediated cytokine production.
650    _2
$a zvířata $7 D000818
650    _2
$a kultivované buňky $7 D002478
650    _2
$a choroidea $x krevní zásobení $x metabolismus $7 D002829
650    _2
$a neovaskularizace choroidey $x metabolismus $x patologie $7 D020256
650    _2
$a cytokiny $x metabolismus $7 D016207
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a erythropoetin $x metabolismus $7 D004921
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a makrofágy $x cytologie $x fyziologie $7 D008264
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a myši $7 D051379
650    _2
$a myši inbrední C57BL $7 D008810
650    _2
$a myši knockoutované $7 D018345
650    _2
$a receptory erythropoetinu $x fyziologie $7 D017467
650    _2
$a signální transdukce $7 D015398
655    _2
$a časopisecké články $7 D016428
655    _2
$a Research Support, N.I.H., Extramural $7 D052061
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Divoky, Vladimir $u Department of Biology, Palacky University, Olomouc, Czech Republic.
700    1_
$a Prchal, Josef T., $u Department of Hematology, University of Utah, Salt Lake City, UT, USA. $d 1945- $7 xx0148595
700    1_
$a Kunz, Eric $u John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA.
700    1_
$a Simmons, Aaron B $u John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA.
700    1_
$a Wang, Haibo $u John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA.
700    1_
$a Hartnett, Mary Elizabeth $u John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA. ME.Hartnett@hsc.utah.edu.
773    0_
$w MED00182195 $t Scientific reports $x 2045-2322 $g Roč. 8, č. 1 (2018), s. 2161
856    41
$u https://pubmed.ncbi.nlm.nih.gov/29391474 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20190107 $b ABA008
991    __
$a 20220512082041 $b ABA008
999    __
$a ok $b bmc $g 1364915 $s 1039070
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 8 $c 1 $d 2161 $e 20180201 $i 2045-2322 $m Scientific reports $n Sci Rep $x MED00182195
LZP    __
$a Pubmed-20190107

Najít záznam

Citační ukazatele

Možnosti archivace