PMID- 36640227
OWN - NLM
STAT- MEDLINE
DCOM- 20230518
LR  - 20230518
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 46
IP  - 3
DP  - 2023 Jun
TI  - Collagen Triple Helix Repeat Containing 1 Deficiency Protects Against Airway 
      Remodeling and Inflammation in Asthma Models In Vivo and In Vitro.
PG  - 925-940
LID - 10.1007/s10753-022-01781-3 [doi]
AB  - Asthma is a chronic inflammatory disease characterized by airway remodeling and 
      lung inflammation. Collagen triple helix repeat containing 1 (CTHRC1), a 
      glycoprotein, is involved in multiple pathological processes, including 
      inflammation and fibrosis. However, the function of CTHRC1 in asthma remains 
      unclear. In the present study, the mouse asthma model was successfully generated 
      by sensitizing and challenging mice with ovalbumin (OVA). CTHRC1 expression at 
      both RNA and protein levels was significantly upregulated in lung tissues of 
      asthmatic mice. Asthmatic mice exhibited significant airway remodeling as 
      evidenced by increased bronchial wall and smooth muscle cell layer thickness, 
      goblet cell hyperplasia and collagen deposition, and epithelial-mesenchymal 
      transition (EMT), but those characteristics were reversed by CTHRC1 silencing. 
      The cell model with transforming growth factor-beta1 (TGF-beta1) induction in bronchial 
      epithelial cells (BEAS-2B) was conducted to verify the effects of CTHRC1 on EMT, 
      a classic mechanism that mediates airway remodeling. The results showed that 
      TGF-beta1 stimulation increased CTHRC1 expression, and CTHRC1 knockdown inhibited 
      TGF-beta1-induced EMT. OVA-treated mice also showed increased inflammatory cell 
      infiltration and the production of OVA-specific immunoglobulin E (IgE), 
      interleukin (IL)-4, IL-5, and IL-13, which were decreased by CTHRC1 
      downregulation. The effects of CTHRC1 on OVA-induced airway inflammation were 
      further determined by treating BEAS-2B cells with IL-13, in which CTHRC1 
      knockdown reduced the IL-13-induced secretion of pro-inflammatory factors, 
      including IL-4 and IL-5. In conclusion, these results indicate that CTHRC1 
      silencing attenuates asthmatic airway remodeling and inflammation in vivo and in 
      vitro, suggesting that CTHRC1 may be a potential target for asthma treatment.
CI  - (c) 2023. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Feng, Yong
AU  - Feng Y
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 36 
      Sanhao Street, Heping District, Liaoning Province, 110004, China.
FAU - Hu, Jiapeng
AU  - Hu J
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 36 
      Sanhao Street, Heping District, Liaoning Province, 110004, China.
FAU - Liu, Fen
AU  - Liu F
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 36 
      Sanhao Street, Heping District, Liaoning Province, 110004, China.
FAU - Shang, Yunxiao
AU  - Shang Y
AUID- ORCID: 0000-0001-9894-6096
AD  - Department of Pediatrics, Shengjing Hospital of China Medical University, 36 
      Sanhao Street, Heping District, Liaoning Province, 110004, China. 
      yunxiaoshang2020@163.com.
LA  - eng
PT  - Journal Article
DEP - 20230114
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-5)
RN  - 9007-34-5 (Collagen)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Transforming Growth Factor beta1/metabolism
MH  - Airway Remodeling
MH  - Interleukin-13
MH  - Interleukin-5
MH  - *Asthma/metabolism
MH  - Inflammation/chemically induced
MH  - Collagen/metabolism
MH  - Ovalbumin/adverse effects
MH  - Disease Models, Animal
MH  - Mice, Inbred BALB C
OTO - NOTNLM
OT  - Airway remodelling
OT  - Asthma
OT  - CTHRC1
OT  - EMT
OT  - Inflammation
EDAT- 2023/01/15 06:00
MHDA- 2023/05/18 06:42
CRDT- 2023/01/14 11:17
PHST- 2022/04/10 00:00 [received]
PHST- 2022/12/28 00:00 [accepted]
PHST- 2022/11/07 00:00 [revised]
PHST- 2023/05/18 06:42 [medline]
PHST- 2023/01/15 06:00 [pubmed]
PHST- 2023/01/14 11:17 [entrez]
AID - 10.1007/s10753-022-01781-3 [pii]
AID - 10.1007/s10753-022-01781-3 [doi]
PST - ppublish
SO  - Inflammation. 2023 Jun;46(3):925-940. doi: 10.1007/s10753-022-01781-3. Epub 2023 
      Jan 14.