## 3 Results
### Deletion of TRPV4 Aggrawates Tunica Media Damage in CaCl\({}_{2}\)-Induced Aortic Injury  
Consistent with the above results, histological analysis of H&E-stained sections revealed an apparent increase in the overall aortic wall thickness of CaCl\({}_{2}\)-treated mice groups compared to sham mice groups. The adventitial layer thickness of the aorta was remarkably higher with an apparent infiltration of immune cells (Figure 3). Moreover, the tunica media of KO-CaCl\({}_{2}\) mice was extensively damaged and detached from the adventitial layer. In addition, CaCl\({}_{2}\)-injured aorta showed more elongation and destruction of the tunica media elastic fibers in KO-CaCl\({}_{2}\) mice compared to WT-CaCl\({}_{2}\) mice (Figure 4).  
Figure 2: TRPV4 limits abdominal aortic aneurysm induced by CaCl\({}_{2}\). (**A**) Representative photographs of infrarenal aortas of WT and TRPV4\(-\)KO mice two weeks after surgery. (**B**) Outer diameter of WT and TRPV4-KO infrarenal aortas two weeks after surgery (WT Sham \(n\) = 8, WT CaCl\({}_{2}\)\(n\) = 14, TRPV\(-\)KO Sham \(n\) = 9, TRPV4\(-\)KO CaCl\({}_{2}\)\(n\) = 15; One\(-\)way ANOVA followed by [PERSON]’s multiple comparison test). Data represent the mean \(\pm\) SD. WT: wild type, TRPV4\(-\)KO: Transient Receptor Channel Vanilloid 4\(-\)Knock out. \(\mathbf{{}^{*}}\) denotes statistical significance.  
Deletion of TRPV4 Intrases Tuncia Media Area and Lumen Circumference in CaCl\({}_{2}\)-Induced Aortic Injury  
To further investigate the morphometric changes in WT and TRPV4-KO mice, we analyzed H&E sections of the infrarenal aorta using additional parameters. The aortic circumference (\(\upmu\)m) and lumen area (\(\upmu\)m\({}^{2}\)) of the TRPV4-KO mice group were significantly higher in CaCl\({}_{2}\) mice compared with sham mice (TRPV4-KO CaCl\({}_{2}\) vs. TRPV4-KO sham: \(p<0.05\); Figure 5A,B). Moreover, tunica media area (\(\upmu\)m\({}^{2}\)) was significantly increased in TRPV4-KO mice after CaCl\({}_{2}\) injury compared to that in sham TRPV4-KO mice. (TRPV4-KO CaCl\({}_{2}\) vs. TRPV4-KO sham: \(p<0.05\), Figure 5C).  
Figure 4: Deletion of TRPV4 induces elongation and destruction of elastic lamellae in CaCl\({}_{2}\)-induced induced aorta injury. Representative fluorescence microscopy images showing the tunica media elastic lamellae in the cross sections of infrarenal aortas of different study groups. The elongation and destruction of elastic lamella of the tunica medial layer are clearly observed in TRPV4\(-\)KO aorta after CaCl\({}_{2}\) injury (Black arrows indicate elongated and destructed elastic lamella) (scale bar: 100 \(\upmu\)m). WT: wild type, TRPV4\(-\)KO: Transient Receptor Channel Vanilloid 4-Knock out.  
Figure 3: Deletion of TRPV4 promotes tunica media damage in CaCl\({}_{2}\)-induced aorta injury. Hematoxylin and Eosin-stained images of cross sections of infrarenal aortas showing an enlarged adventitial layer with remarkable infiltration of immune cells after CaCl\({}_{2}\) injury (Black arrows indicate infiltrated immune cells) (scale bar: 100 \(\upmu\)m). WT: wild type, TRPV4\(-\)KO: Transient Receptor Channel Vanilloid 4\(-\)Knock out.  
Figure 5: Deletion of TRPV4 increases tunica media area, lumen circumference, and lumen area in CaCl\({}_{2}-\)induced aorta injury. (**A**) Circumference area. (**B**) Lumen area. (**C**) Medial layer area of WT WT  
and KO infrarenal aortas from Hematoxylin and Eosin-stained images of cross sections of infrarenal aortas. TRPV4\(-\)KO showed a significant increase in tunica media area, lumen circumference, and lumen area after CaCl\({}_{2}\) injury. One-way ANOVA followed by [PERSON]'s multiple comparison test (WT Sham \(n=9\), WT CaCl\({}_{2}\)\(n=14\), TRPV\(-\)KO Sham \(n=6\), TRPV4\(-\)KO CaCl\({}_{2}\)\(n=13\)). WT: wild type, TRPV4-KO: Transient Receptor Channel Vanilloid 4\(-\)Knock out. \({}^{\star\star}\) denotes statistical significance.