PMID- 34761651
OWN - NLM
STAT- MEDLINE
DCOM- 20220210
LR  - 20220210
IS  - 1578-1267 (Electronic)
IS  - 0301-0546 (Linking)
VI  - 49
IP  - 6
DP  - 2021
TI  - SEMA3A protects against hyperoxia-induced lung injury in a bronchopulmonary 
      dysplasia model of newborn rat by inhibiting ERK pathway.
PG  - 8-15
LID - 10.15586/aei.v49i6.478 [doi]
AB  - BACKGROUND: Hyperoxia induces lung injury through lung inflammation in premature 
      infants, leading to bronchopulmonary dysplasia (BPD). Semaphorin 3A (SEMA3A) 
      participates in diverse biological processes, including cell migration, 
      angiogenesis, and inflammation. The effect of SEMA3A on hyperoxic lung injury of 
      neonatal rats with BPD was investigated in this study. METHODS: Neonatal rats 
      with BPD were established through hyperoxia treatment. Hematoxylin-eosin staining 
      was used to evaluate histopathological analysis in lung tissues. SEMA3A 
      expression was assessed by reverse transcription-quantitative polymerase chain 
      reaction (RT-qPCR) and western blot assay. Adeno-associated virus (AAV)-mediated 
      over-expression of SEMA3A (AAV-SEMA3A) was administrated into hyperoxia-induced 
      rats, and apoptosis was evaluated by TUNEL staining. Levels of inflammatory 
      cytokines were investigated by enzyme-linked-immunosorbent serologic assay 
      (ELISA). RESULTS: Hyperoxia-induced histopathological changes in lung tissue 
      reduced alveolar number and enhanced alveolar interval and alveolar volume. 
      SEMA3A was downregulated in lung tissue of hyperoxia-induced rats. AAV-SEMA3A 
      injection attenuated hyperoxia-induced cell apoptosis in lung tissues by 
      increasing Bcl-2 and decreasing Bax and cleaved caspase-3. Moreover, the enhanced 
      levels of Interleukin (IL)-1beta, monocyte chemoattractant protein (MCP)-1, and 
      tumor necrosis factor-alpha (TNF-alpha) in hyperoxia-induced rats were restored by 
      AAV-SEMA3A injection by the downregulation of nuclear factor kappa B (NF-kappaB) 
      phosphorylation. AAV-SEMA3A injection also ameliorated histopathological changes 
      in lung tissues of hyperoxia-induced rats by increasing the number of radial 
      alveolar count and decreasing the volume of mean linear intercept. Besides, the 
      protein expression levels of extracellular signal-regulated kinase (ERK) and 
      c-Jun N-terminal kinase (JNK) phosphorylation were reduced in hyperoxia-induced 
      rats post-AAV-SEMA3A injection. CONCLUSION: Ectopical expression of SEMA3A 
      suppressed hyperoxia-induced apoptosis and inflammation in neonatal rats, and 
      ameliorated the histopathological changes through inactivation of ERK/JNK 
      pathway.
FAU - Liang, Zhenyu
AU  - Liang Z
AD  - Department of Pediatrics, Guangdong Second Provincial General Hospital, Guangdong 
      Province, China.
FAU - Zhang, Xiao
AU  - Zhang X
AD  - Department of Pediatrics, Guangdong Second Provincial General Hospital, Guangdong 
      Province, China.
FAU - Liu, Yingxian
AU  - Liu Y
AD  - Department of Pediatrics, Guangdong Second Provincial General Hospital, Guangdong 
      Province, China.
FAU - Wu, Qianmei
AU  - Wu Q
AD  - Department of Pediatrics, Guangdong Second Provincial General Hospital, Guangdong 
      Province, China.
FAU - You, Chuming
AU  - You C
AD  - Department of Pediatrics, Guangdong Second Provincial General Hospital, Guangdong 
      Province, China; youchuming@163.com.
LA  - eng
PT  - Journal Article
DEP - 20211101
PL  - Singapore
TA  - Allergol Immunopathol (Madr)
JT  - Allergologia et immunopathologia
JID - 0370073
RN  - 0 (Sema3a protein, rat)
RN  - 0 (Semaphorin-3A)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - *Bronchopulmonary Dysplasia/therapy
MH  - Disease Models, Animal
MH  - Extracellular Signal-Regulated MAP Kinases
MH  - *Hyperoxia
MH  - Inflammation
MH  - Lung
MH  - *Lung Injury
MH  - MAP Kinase Signaling System
MH  - Rats
MH  - *Semaphorin-3A/genetics
OTO - NOTNLM
OT  - ERK/JNK
OT  - SEMA3A
OT  - apoptosis
OT  - bronchopulmonary dysplasia
OT  - hyperoxia
OT  - inflammation
OT  - lung injury
EDAT- 2021/11/12 06:00
MHDA- 2022/02/11 06:00
CRDT- 2021/11/11 07:28
PHST- 2021/07/09 00:00 [received]
PHST- 2021/08/21 00:00 [accepted]
PHST- 2021/11/11 07:28 [entrez]
PHST- 2021/11/12 06:00 [pubmed]
PHST- 2022/02/11 06:00 [medline]
AID - 10.15586/aei.v49i6.478 [doi]
PST - epublish
SO  - Allergol Immunopathol (Madr). 2021 Nov 1;49(6):8-15. doi: 10.15586/aei.v49i6.478. 
      eCollection 2021.