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SOX11 is a critical biomarker for mantle cell lymphoma (MCL) diagnosis; however, its role remains unclear in MCL. Here, clinical-pathological analysis showed Ki67 index was negatively relevant to SOX11 expression only in CD43 positive cases. Coexpression of SOX11/CD43 indicated longer overall survival. In vitro, knockout/overexpression of SOX11 or CD43 promoted/inhibited cell proliferation respectively. CD43 overexpression reversed tumor proliferation induced by SOX11 knockdown. Furthermore, overexpressing/silencing the SOX11/CD43 gene affects phosphorylation of p38-MAPK while p38 inhibitor reversed proliferation induced by si-SOX11 or si-CD43, respectively. In CAM-DR model, both SOX11 and CD43 in MCL cells were elevated when co-cultured with M2-10B4 bone marrow fibroblasts or fibronectin. Knockdown/overexpression of SOX11 decreased/increased cell adhesion, respectively, and the effect induced by silencing SOX11 was reversed by overexpression of CD43. Collectively, SOX11 could inhibit tumor proliferation and promote CAM-DR in a CD43 dependent manner.

Background To establish a decision model based on two- (2D) and three-dimensional (3D) eye data of patients with ptosis for developing personalized surgery plans. Methods Data of this retrospective, case-control study was collected from March 2019 to June 2019 at the Department of Ophthalmology, Shanghai Ninth People’s Hospital, and then the patients were followed up for 3 months. One hundred fifty-two complete feature eyes from 100 voluntary patients with ptosis and satisfactory surgical results were selected, with 48 eyes excluded due to any severe condition or improper collection and shooting angle. Three experimental schemes were set as follows: use 2D distance alone, use 3D distance alone, and use two distances at the same time. The five most common evaluation indicators used in the binary classification problem to test the decision model were accuracy (ACC), precision, recall, F1-score, and area under the curve (AUC). Results For diagnostic discrimination, recall of “3D”, “2D” and “Both” schemes were 0.875, 0.875 and 0.938 respectively. And precision of the three schemes were 0.8333, 0.7778 and 1.0000 for the surgical procedure classification. Values of “Both” scheme that combined 2D and 3D data were the highest in two classifications. Conclusions In this study, 3D eye data are introduced into clinical practice to construct a decision model for ptosis surgery. Our decision model presents exceptional prediction effect, especially when 2D and 3D data employed jointly.

CXC chemokine family has been related to atherogenesis for long. However, the relationship between CXCL14 and atherogenesis is still unclear. This study preliminarily detected CXCL14 expression at foam cells in atherosclerosis specimens by immunohistochemistry. In vitro foam cells were derived from THP-1 after phorbol-12-myristate-13-acetate (PMA) and oxidized low-density lipoprotein (ox-LDL) stimulation. Immunoblotting and qPCR convinced CXCL14 expression variation during foam cell formation. We further demonstrated that ox-LDL regulated CXCL14 expression by AP-1. AP-1 could bind to CXCL14 promoter and up-regulate CXCL14 mRNA expression. Besides, CXCL14 promoted THP-1 migration, macrophage lipid phagocytosis, and smooth muscle cell migration as well as proliferation mainly via the ERK1/2 pathway. Additionally, a CXCL14 peptide-induced immune therapy showed efficacy in ApoE-/- mouse model. In conclusion, our study demonstrated that CXCL14 is highly up-regulated during foam cell formation and promotes atherogenesis in various ways. CXCL14 may be a potent therapeutic target for atherosclerosis.

C-kit positive cardiac stem cells (CSCs) have been shown to contribute to myocardial regeneration after infarction. Previously, we have shown that the c-kit ligand stem cell factor (SCF) can induce CSC migration into the infarcted area during myocardial infarction (MI). However, the precise mechanism involved is not fully understood. In this study, we found that CSCs also express C-X-C chemokine receptor type 4 (CXCR4), which is a typical member of the seven transmembrane-spanning G protein-coupled receptor (GPCR). In vitro, activation of c-kit signalling by SCF promotes migration of CSCs with increased phosphorylation of CXCR4-serine 339, p38 mitogen-activated protein kinase (p38 MAPK) and extracellular regulated protein kinases 1/2 (ERK1/2). Knockdown of CXCR4 expression by siRNA reduces SCF/c-kit-induced migration and downstream signalling. As previously reported, CXCR4-serine 339 phosphorylation is mainly regulated by GPCR kinase 6 (GRK6); thus, silencing of GRK6 expression by siRNA impairs CXCR4-serine 339 phosphorylation and migration of CSCs caused by SCF. In vivo, knockdown of GRK6 impairs the ability of CSCs to migrate into peri-infarcted areas. These results demonstrate that SCF-induced CSC migration is regulated by the transactivation of CXCR4-serine 339 phosphorylation, which is mediated by GRK6.