Aggravated pulmonary injury after subarachnoid hemorrhage in PDGF-Bret/ret mice
| Autor: | Jie Qu, Yujie Chen, Hua Feng, Pengyu Pan, Qiang Li, Shilun Zuo, Yang Yang, Rongwei Li, Xin Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Pathology Subarachnoid hemorrhage Neurology medicine.medical_treatment lcsh:Surgery Neuroprotection lcsh:RC346-429 03 medical and health sciences 0302 clinical medicine medicine cardiovascular diseases lcsh:Neurology. Diseases of the nervous system biology business.industry Growth factor lcsh:RD1-811 medicine.disease Pathophysiology nervous system diseases 030104 developmental biology medicine.anatomical_structure Pulmonary injury biology.protein Surgery Neurology (clinical) Neurosurgery Pericyte Lung-specific surfactant protein Platelet-derived growth factor B business 030217 neurology & neurosurgery Platelet-derived growth factor receptor |
| Zdroj: | Chinese Neurosurgical Journal, Vol 6, Iss 1, Pp 1-9 (2020) |
| ISSN: | 2057-4967 |
| DOI: | 10.1186/s41016-020-00193-2 |
| Popis: | Background Recent advances in surgical and neuroprotective strategies could effectively manage the pathophysiological progression of subarachnoid hemorrhage (SAH). However, pulmonary dysfunction frequently occurs in SAH patients with an increased risk of unsatisfactory outcomes. Based on the similar microvascular structures in the blood-air barrier and blood-brain barrier and possible brain-lung crosstalks, we believe that pericytes may be involved in both neurological and pulmonary dysfunction after SAH. Methods In our experiments, platelet-derived growth factor B (PDGF-B) retention motif knockout (PDGF-Bret/ret) mice and adeno-associated virus PDGF-B were employed to show the involvement of pericyte deficiency and PDGF-B expression. Neurological score, SAH grade, hematoxylin-eosin staining, and PaO2/FiO2 ratio analysis were performed to evaluate the neurological deficits and pulmonary functions in endovascular perforation SAH models at 24 h after surgery, as well as western blotting and immunofluorescence staining for underlying molecular expressions. Results We found that neonatal PDGF-Bret/ret mice exhibited pulmonary atelectasis 12 h after birth. Further investigation showed a decrease in PaO2/FiO2 and lung-specific surfactant proteins in adult PDGF-Bret/ret mice. These dysfunctions were much worse than those in wild-type mice at 24 h after SAH. PDGF-B overexpression alleviated pulmonary dysfunction after SAH. Conclusions These results suggested pulmonary dysfunction after SAH and the pivotal role of PDGF-B signaling for the pathophysiological process and future therapeutic targets of pulmonary injury treatment after SAH. Further studies are needed for pathophysiological investigations and translational studies on pulmonary injuries after SAH. |
| Databáze: | OpenAIRE |
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