Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes
It is postulated that central effects of angiotensin (Ang) II may be indirect due to rapid conversion to Ang III by aminopeptidase A (APA). Previously, we showed that Ang II and Ang III induced mitogen-activated protein (MAP) kinases ERK1/2 and stress-activated protein kinase/Jun-terminal kinases (S...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2013-01-01
|
| Series: | International Journal of Hypertension |
| Online Access: | http://dx.doi.org/10.1155/2013/782861 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832561106104614912 |
|---|---|
| author | Michelle A. Clark Chinh Nguyen Hieu Tran |
| author_facet | Michelle A. Clark Chinh Nguyen Hieu Tran |
| author_sort | Michelle A. Clark |
| collection | DOAJ |
| description | It is postulated that central effects of angiotensin (Ang) II may be indirect due to rapid conversion to Ang III by aminopeptidase A (APA). Previously, we showed that Ang II and Ang III induced mitogen-activated protein (MAP) kinases ERK1/2 and stress-activated protein kinase/Jun-terminal kinases (SAPK/JNK) phosphorylation in cultured rat astrocytes. Most importantly, both peptides were equipotent in causing phosphorylation of these MAP kinases. In these studies, we used brainstem and cerebellum astrocytes to determine whether Ang II’s phosphorylation of these MAP kinases is due to the conversion of the peptide to Ang III. We pretreated astrocytes with 10 μM amastatin A or 100 μM glutamate phosphonate, selective APA inhibitors, prior to stimulating with either Ang II or Ang III. Both peptides were equipotent in stimulating ERK1/2 and SAPK/JNK phosphorylation. The APA inhibitors failed to prevent Ang II- and Ang III-mediated phosphorylation of the MAP kinases. Further, pretreatment of astrocytes with the APA inhibitors did not affect Ang II- or Ang III-induced astrocyte growth. These findings suggest that both peptides directly induce phosphorylation of these MAP kinases as well as induce astrocyte growth. These studies establish both peptides as biologically active with similar intracellular and physiological effects. |
| format | Article |
| id | doaj-art-a02c4f7baa97466b8250230e15dd39f1 |
| institution | Kabale University |
| issn | 2090-0384 2090-0392 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Hypertension |
| spelling | doaj-art-a02c4f7baa97466b8250230e15dd39f12025-02-03T01:25:54ZengWileyInternational Journal of Hypertension2090-03842090-03922013-01-01201310.1155/2013/782861782861Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat AstrocytesMichelle A. Clark0Chinh Nguyen1Hieu Tran2Department of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL 33328, USADepartment of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL 33328, USADepartment of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL 33328, USAIt is postulated that central effects of angiotensin (Ang) II may be indirect due to rapid conversion to Ang III by aminopeptidase A (APA). Previously, we showed that Ang II and Ang III induced mitogen-activated protein (MAP) kinases ERK1/2 and stress-activated protein kinase/Jun-terminal kinases (SAPK/JNK) phosphorylation in cultured rat astrocytes. Most importantly, both peptides were equipotent in causing phosphorylation of these MAP kinases. In these studies, we used brainstem and cerebellum astrocytes to determine whether Ang II’s phosphorylation of these MAP kinases is due to the conversion of the peptide to Ang III. We pretreated astrocytes with 10 μM amastatin A or 100 μM glutamate phosphonate, selective APA inhibitors, prior to stimulating with either Ang II or Ang III. Both peptides were equipotent in stimulating ERK1/2 and SAPK/JNK phosphorylation. The APA inhibitors failed to prevent Ang II- and Ang III-mediated phosphorylation of the MAP kinases. Further, pretreatment of astrocytes with the APA inhibitors did not affect Ang II- or Ang III-induced astrocyte growth. These findings suggest that both peptides directly induce phosphorylation of these MAP kinases as well as induce astrocyte growth. These studies establish both peptides as biologically active with similar intracellular and physiological effects.http://dx.doi.org/10.1155/2013/782861 |
| spellingShingle | Michelle A. Clark Chinh Nguyen Hieu Tran Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes International Journal of Hypertension |
| title | Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes |
| title_full | Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes |
| title_fullStr | Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes |
| title_full_unstemmed | Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes |
| title_short | Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes |
| title_sort | distinct molecular effects of angiotensin ii and angiotensin iii in rat astrocytes |
| url | http://dx.doi.org/10.1155/2013/782861 |
| work_keys_str_mv | AT michelleaclark distinctmoleculareffectsofangiotensiniiandangiotensiniiiinratastrocytes AT chinhnguyen distinctmoleculareffectsofangiotensiniiandangiotensiniiiinratastrocytes AT hieutran distinctmoleculareffectsofangiotensiniiandangiotensiniiiinratastrocytes |