title: Increased immunohistochemical expression of YKL-40 in the spleen of patients with portal hypertension.
abstract: YKL-40 has been identified as a growth factor in connective tissue cells and also a migration factor in vascular smooth muscle cells. To a large extent, the increase of serum YKL-40 is attributed to liver fibrosis and asthma. However, the relationship of the expression and clinical/prognostic significance of YKL-40 to the splenomegaly of patients with portal hypertension is unclear. In the present study, the expression of YKL-40 was studied by immunohistochemistry in 48 splenomegaly tissue samples from patients with portal hypertension and in 14 normal spleen specimens. All specimens were quickly stored at -80°C after resection. Primary antibodies YKL-40 (1:150 dilution, rabbit polyclonal IgG) and MMP-9 (1:200 dilution, rabbit monoclonal IgG) and antirabbit immunoglobulins (HRP K4010) were used in this study. The relationship of clinicopathologic features with YKL-40 is presented. The expression of YKL-40 indicated by increased immunochemical reactivity was significantly up-regulated in splenomegaly tissues compared to normal spleen tissues. Overexpression of YKL-40 was found in 68.8% of splenomegaly tissues and was significantly associated with Child-Pugh classification (P = 0.000), free portal pressure (correlation coefficient = 0.499, P < 0.01) and spleen fibrosis (correlation coefficient = 0.857, P < 0.01). Further study showed a significant correlation between YKL-40 and MMP-9 (correlation coefficient = -0.839, P < 0.01), indicating that YKL-40 might be an accelerator of spleen tissue remodeling by inhibiting the expression of MMP-9. In conclusion, YKL-40 is an important factor involved in the remodeling of spleen tissue of portal hypertension patients and can be used as a therapeutic target for splenomegaly.
authors.affiliation: Department of General Surgery, The Second Affiliated Hospital, Fourth Military Medical University, 1 Xin Xi Road, Xi'an, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Wang
authors.forename: Jian-Guo
authors.initials: JG
authors.lastname: Lu
authors.forename: Qing
authors.initials: Q
authors.lastname: Wang
authors.forename: Xi-Lin
authors.initials: XL
authors.lastname: Du
authors.forename: Rui
authors.initials: R
authors.lastname: Dong
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.forename: Lei
authors.initials: L
authors.lastname: Zhao
authors.forename: Xue
authors.initials: X
authors.lastname: Jiang
authors.forename: Li-Juan
authors.initials: LJ
authors.lastname: Yuan
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D000071451:Chitinase-3-Like Protein 1; D005260:Female; D006801:Humans; D006975:Hypertension, Portal / Q000150:complications / Q000378:metabolism*; D037102:Lectins / Q000378:metabolism*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D008875:Middle Aged; D011817:Rabbits; D013154:Spleen / Q000378:metabolism*; D013163:Splenomegaly / Q000209:etiology / Q000378:metabolism*; D055815:Young Adult
chemical_list: D054392:Adipokines; D015415:Biomarkers; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D037102:Lectins; D020780:Matrix Metalloproteinase 9