Eintrag weiter verarbeiten
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension
Gespeichert in:
| Zeitschriftentitel: | American Journal of Physiology-Renal Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | American Journal of Physiology-Renal Physiology, 310, 2016, 11, S. F1356-F1365 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. |
|---|---|
| author |
Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. |
| spellingShingle |
Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. American Journal of Physiology-Renal Physiology The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension Physiology |
| author_sort |
weiss, sebastian |
| spelling |
Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00040.2016 <jats:p>Adaptive and innate immune responses contribute to hypertension and hypertensive end-organ damage. Here, we determined the role of anaphylatoxin C5a, a major inflammatory effector of the innate immune system that is generated in response to complement activation, in hypertensive end-organ damage. For this purpose, we assessed the phenotype of C5a receptor 1 (C5aR1)-deficient mice in ANG II-induced renal and cardiac injury. Expression of C5aR1 on infiltrating and resident renal as well as cardiac cells was determined using a green fluorescent protein (GFP)-C5aR1 reporter knockin mouse. Flow cytometric analysis of leukocytes isolated from the kidney of GFP-C5aR1 reporter mice showed that 28% of CD45-positive cells expressed C5aR1. Dendritic cells were identified as the major C5aR1-expressing population (88.5%) followed by macrophages and neutrophils. Using confocal microscopy, we detected C5aR1 in the kidney mainly on infiltrating cells. In the heart, only infiltrating cells stained C5aR1 positive. To evaluate the role of C5aR1 deficiency in hypertensive injury, an aggravated model of hypertension was used. Unilateral nephrectomy was performed followed by infusion of ANG II (1.5 ng·g<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>) and salt in wild-type ( n = 34) and C5aR1-deficient mice ( n = 32). C5aR1-deficient mice exhibited less renal injury, as evidenced by significantly reduced albuminuria. In contrast, cardiac injury was accelerated with significantly increased cardiac fibrosis and heart weight in C5aR1-deficient mice after ANG II infusion. No effect was found on blood pressure. In summary, the C5a:C5aR1 axis drives end-organ damage in the kidney but protects from the development of cardiac fibrosis and hypertrophy in experimental ANG II-induced hypertension.</jats:p> The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension American Journal of Physiology-Renal Physiology |
| doi_str_mv |
10.1152/ajprenal.00040.2016 |
| facet_avail |
Online Free |
| finc_class_facet |
Biologie |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1Mi9hanByZW5hbC4wMDA0MC4yMDE2 |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1Mi9hanByZW5hbC4wMDA0MC4yMDE2 |
| institution |
DE-Ch1 DE-L229 DE-D275 DE-Bn3 DE-Brt1 DE-Zwi2 DE-D161 DE-Gla1 DE-Zi4 DE-15 DE-Pl11 DE-Rs1 DE-105 DE-14 |
| imprint |
American Physiological Society, 2016 |
| imprint_str_mv |
American Physiological Society, 2016 |
| issn |
1931-857X 1522-1466 |
| issn_str_mv |
1931-857X 1522-1466 |
| language |
English |
| mega_collection |
American Physiological Society (CrossRef) |
| match_str |
weiss2016thecomplementreceptorc5ar1contributestorenaldamagebutprotectstheheartinangiotensiniiinducedhypertension |
| publishDateSort |
2016 |
| publisher |
American Physiological Society |
| recordtype |
ai |
| record_format |
ai |
| series |
American Journal of Physiology-Renal Physiology |
| source_id |
49 |
| title |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_unstemmed |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_full |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_fullStr |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_full_unstemmed |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_short |
The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_sort |
the complement receptor c5ar1 contributes to renal damage but protects the heart in angiotensin ii-induced hypertension |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1152/ajprenal.00040.2016 |
| publishDate |
2016 |
| physical |
F1356-F1365 |
| description |
<jats:p>Adaptive and innate immune responses contribute to hypertension and hypertensive end-organ damage. Here, we determined the role of anaphylatoxin C5a, a major inflammatory effector of the innate immune system that is generated in response to complement activation, in hypertensive end-organ damage. For this purpose, we assessed the phenotype of C5a receptor 1 (C5aR1)-deficient mice in ANG II-induced renal and cardiac injury. Expression of C5aR1 on infiltrating and resident renal as well as cardiac cells was determined using a green fluorescent protein (GFP)-C5aR1 reporter knockin mouse. Flow cytometric analysis of leukocytes isolated from the kidney of GFP-C5aR1 reporter mice showed that 28% of CD45-positive cells expressed C5aR1. Dendritic cells were identified as the major C5aR1-expressing population (88.5%) followed by macrophages and neutrophils. Using confocal microscopy, we detected C5aR1 in the kidney mainly on infiltrating cells. In the heart, only infiltrating cells stained C5aR1 positive. To evaluate the role of C5aR1 deficiency in hypertensive injury, an aggravated model of hypertension was used. Unilateral nephrectomy was performed followed by infusion of ANG II (1.5 ng·g<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>) and salt in wild-type ( n = 34) and C5aR1-deficient mice ( n = 32). C5aR1-deficient mice exhibited less renal injury, as evidenced by significantly reduced albuminuria. In contrast, cardiac injury was accelerated with significantly increased cardiac fibrosis and heart weight in C5aR1-deficient mice after ANG II infusion. No effect was found on blood pressure. In summary, the C5a:C5aR1 axis drives end-organ damage in the kidney but protects from the development of cardiac fibrosis and hypertrophy in experimental ANG II-induced hypertension.</jats:p> |
| container_issue |
11 |
| container_start_page |
0 |
| container_title |
American Journal of Physiology-Renal Physiology |
| container_volume |
310 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792343172474470405 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T16:46:48.941Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=The+complement+receptor+C5aR1+contributes+to+renal+damage+but+protects+the+heart+in+angiotensin+II-induced+hypertension&rft.date=2016-06-01&genre=article&issn=1522-1466&volume=310&issue=11&pages=F1356-F1365&jtitle=American+Journal+of+Physiology-Renal+Physiology&atitle=The+complement+receptor+C5aR1+contributes+to+renal+damage+but+protects+the+heart+in+angiotensin+II-induced+hypertension&aulast=Wenzel&aufirst=Ulrich+O.&rft_id=info%3Adoi%2F10.1152%2Fajprenal.00040.2016&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792343172474470405 |
| author | Weiss, Sebastian, Rosendahl, Alva, Czesla, Daniel, Meyer-Schwesinger, Catherine, Stahl, Rolf A. K., Ehmke, Heimo, Kurts, Christian, Zipfel, Peter F., Köhl, Jörg, Wenzel, Ulrich O. |
| author_facet | Weiss, Sebastian, Rosendahl, Alva, Czesla, Daniel, Meyer-Schwesinger, Catherine, Stahl, Rolf A. K., Ehmke, Heimo, Kurts, Christian, Zipfel, Peter F., Köhl, Jörg, Wenzel, Ulrich O., Weiss, Sebastian, Rosendahl, Alva, Czesla, Daniel, Meyer-Schwesinger, Catherine, Stahl, Rolf A. K., Ehmke, Heimo, Kurts, Christian, Zipfel, Peter F., Köhl, Jörg, Wenzel, Ulrich O. |
| author_sort | weiss, sebastian |
| container_issue | 11 |
| container_start_page | 0 |
| container_title | American Journal of Physiology-Renal Physiology |
| container_volume | 310 |
| description | <jats:p>Adaptive and innate immune responses contribute to hypertension and hypertensive end-organ damage. Here, we determined the role of anaphylatoxin C5a, a major inflammatory effector of the innate immune system that is generated in response to complement activation, in hypertensive end-organ damage. For this purpose, we assessed the phenotype of C5a receptor 1 (C5aR1)-deficient mice in ANG II-induced renal and cardiac injury. Expression of C5aR1 on infiltrating and resident renal as well as cardiac cells was determined using a green fluorescent protein (GFP)-C5aR1 reporter knockin mouse. Flow cytometric analysis of leukocytes isolated from the kidney of GFP-C5aR1 reporter mice showed that 28% of CD45-positive cells expressed C5aR1. Dendritic cells were identified as the major C5aR1-expressing population (88.5%) followed by macrophages and neutrophils. Using confocal microscopy, we detected C5aR1 in the kidney mainly on infiltrating cells. In the heart, only infiltrating cells stained C5aR1 positive. To evaluate the role of C5aR1 deficiency in hypertensive injury, an aggravated model of hypertension was used. Unilateral nephrectomy was performed followed by infusion of ANG II (1.5 ng·g<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>) and salt in wild-type ( n = 34) and C5aR1-deficient mice ( n = 32). C5aR1-deficient mice exhibited less renal injury, as evidenced by significantly reduced albuminuria. In contrast, cardiac injury was accelerated with significantly increased cardiac fibrosis and heart weight in C5aR1-deficient mice after ANG II infusion. No effect was found on blood pressure. In summary, the C5a:C5aR1 axis drives end-organ damage in the kidney but protects from the development of cardiac fibrosis and hypertrophy in experimental ANG II-induced hypertension.</jats:p> |
| doi_str_mv | 10.1152/ajprenal.00040.2016 |
| facet_avail | Online, Free |
| finc_class_facet | Biologie |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1Mi9hanByZW5hbC4wMDA0MC4yMDE2 |
| imprint | American Physiological Society, 2016 |
| imprint_str_mv | American Physiological Society, 2016 |
| institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14 |
| issn | 1931-857X, 1522-1466 |
| issn_str_mv | 1931-857X, 1522-1466 |
| language | English |
| last_indexed | 2024-03-01T16:46:48.941Z |
| match_str | weiss2016thecomplementreceptorc5ar1contributestorenaldamagebutprotectstheheartinangiotensiniiinducedhypertension |
| mega_collection | American Physiological Society (CrossRef) |
| physical | F1356-F1365 |
| publishDate | 2016 |
| publishDateSort | 2016 |
| publisher | American Physiological Society |
| record_format | ai |
| recordtype | ai |
| series | American Journal of Physiology-Renal Physiology |
| source_id | 49 |
| spelling | Weiss, Sebastian Rosendahl, Alva Czesla, Daniel Meyer-Schwesinger, Catherine Stahl, Rolf A. K. Ehmke, Heimo Kurts, Christian Zipfel, Peter F. Köhl, Jörg Wenzel, Ulrich O. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00040.2016 <jats:p>Adaptive and innate immune responses contribute to hypertension and hypertensive end-organ damage. Here, we determined the role of anaphylatoxin C5a, a major inflammatory effector of the innate immune system that is generated in response to complement activation, in hypertensive end-organ damage. For this purpose, we assessed the phenotype of C5a receptor 1 (C5aR1)-deficient mice in ANG II-induced renal and cardiac injury. Expression of C5aR1 on infiltrating and resident renal as well as cardiac cells was determined using a green fluorescent protein (GFP)-C5aR1 reporter knockin mouse. Flow cytometric analysis of leukocytes isolated from the kidney of GFP-C5aR1 reporter mice showed that 28% of CD45-positive cells expressed C5aR1. Dendritic cells were identified as the major C5aR1-expressing population (88.5%) followed by macrophages and neutrophils. Using confocal microscopy, we detected C5aR1 in the kidney mainly on infiltrating cells. In the heart, only infiltrating cells stained C5aR1 positive. To evaluate the role of C5aR1 deficiency in hypertensive injury, an aggravated model of hypertension was used. Unilateral nephrectomy was performed followed by infusion of ANG II (1.5 ng·g<jats:sup>−1</jats:sup>·min<jats:sup>−1</jats:sup>) and salt in wild-type ( n = 34) and C5aR1-deficient mice ( n = 32). C5aR1-deficient mice exhibited less renal injury, as evidenced by significantly reduced albuminuria. In contrast, cardiac injury was accelerated with significantly increased cardiac fibrosis and heart weight in C5aR1-deficient mice after ANG II infusion. No effect was found on blood pressure. In summary, the C5a:C5aR1 axis drives end-organ damage in the kidney but protects from the development of cardiac fibrosis and hypertrophy in experimental ANG II-induced hypertension.</jats:p> The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension American Journal of Physiology-Renal Physiology |
| spellingShingle | Weiss, Sebastian, Rosendahl, Alva, Czesla, Daniel, Meyer-Schwesinger, Catherine, Stahl, Rolf A. K., Ehmke, Heimo, Kurts, Christian, Zipfel, Peter F., Köhl, Jörg, Wenzel, Ulrich O., American Journal of Physiology-Renal Physiology, The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension, Physiology |
| title | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_full | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_fullStr | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_full_unstemmed | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_short | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| title_sort | the complement receptor c5ar1 contributes to renal damage but protects the heart in angiotensin ii-induced hypertension |
| title_unstemmed | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension |
| topic | Physiology |
| url | http://dx.doi.org/10.1152/ajprenal.00040.2016 |