Zhengquan Yu

First Affiliated Hospital of Zhengzhou University

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Maksim V. Plikus

University of California, Irvine

Cong Lv

China Agricultural University

Fazheng Ren

China Agricultural University

Jiuzhi Xu

China Agricultural University

Christopher J. Lengner

University of Pennsylvania

Qingyong Meng

China Agricultural University

Yuhua Tian

Zhengzhou University

Xiaole Sheng

Zhejiang University

Yongli Song

Air Force Medical University

Bogi Andersen

University of California, Irvine

Cooperative Institutions

China Agricultural University

216

University of California, Irvine

106

Chinese Academy of Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

University of Chinese Academy of Sciences

Soochow University

Peking University

Sun Yat-sen University

Ministry of Agriculture and Rural Affairs

University of Pennsylvania

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Mucin Binding Protein of Lactobacillus casei Inhibits HT-29 Colorectal Cancer Cell Proliferation

Nutrients (2023)

Xuan Ju Xi Wu Yukun Chen Shanshan Cui Zixuan Cai

Many Lactobacillus casei strains are reported to exhibit anti-proliferative effects on colorectal cancer cells; however, the mechanism remains largely unknown. While there has been considerable interest in bacterial small metabolites such as short chain fatty acids, prior reports suggested that larger-sized molecules mediate the anti-proliferative effect of L. casei. Here, other possible ways of communication between gut bacteria and its host are investigated. LevH1 is a protein displayed on the surface of L. casei, and its mucin binding domain is highly conserved. Based on previous reports that the cell-free supernatant fractions decreased colorectal cell proliferation, we cloned the mucin binding domain of the LevH1 protein, expressed and purified this mucin binding protein (MucBP). It has a molecular weight of 10 kDa, is encoded by a 250 bp gene, and is composed primarily of a β-strand, β-turns, and random coils. The amino acid sequence is conserved while the 36th amino acid residue is arginine in L. casei CAUH35 and serine in L. casei IAM1045, LOCK919, 12A, and Zhang. MucBP36R exhibited dose-dependent anti-proliferative effects against HT-29 cells while a mutation of 36S abolished this activity. Predicted structures suggest that this mutation slightly altered the protein structure, thus possibly affecting subsequent communication with HT-29 cells. Our study identified a novel mode of communication between gut bacteria and their host.

Lactobacillus casei

10.3390/nu15102314

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Citations (4)

Cycling Stem Cells Are Radioresistant and Regenerate the Intestine

Cell Reports (2020)

Xiaole Sheng Ziguang Lin Cong Lv Chunlei Shao Xueyun Bi

A certain number of epithelial cells in intestinal crypts are DNA damage resistant and contribute to regeneration. However, the cellular mechanism underlying intestinal regeneration remains unclear. Using lineage tracing, we show that cells marked by an Msi1 reporter (Msi1+) are right above Lgr5high cells in intestinal crypts and exhibit DNA damage resistance. Single-cell RNA sequencing reveals that the Msi1+ cells are heterogeneous with the majority being intestinal stem cells (ISCs). The DNA damage-resistant subpopulation of Msi1+ cells is characterized by low-to-negative Lgr5 expression and is more rapidly cycling than Lgr5high radiosensitive crypt base columnar stem cells (CBCs). This enables an efficient repopulation of the intestinal epithelium at early stage when Lgr5high cells are not emerging. Furthermore, relative to CBCs, Msi1+ cells preferentially produce Paneth cells during homeostasis and upon radiation repair. Together, we demonstrate that the DNA damage-resistant Msi1+ cells are cycling ISCs that maintain and regenerate the intestinal epithelium.

LGR5

Intestinal epithelium

Radioresistance

Paneth cell

Intestinal mucosa

10.1016/j.celrep.2020.107952

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Citations (51)

Additional file 5: of A de novo silencer causes elimination of MITF-M expression and profound hearing loss in pigs

Figshare (2016)

Lei Chen Weiwei Guo Lili Ren Mingyao Yang Yaofeng Zhao

Supporting data. 1 Data of ABR tests (pigs). 2 Data of EP. 3 Data of K+ concentration. 4 Data of Mitf exon fold change. 5 Data of reporter assay. 6 Data of ABR tests (mice). 7 Data of mouse Mitf qPCR (Ct). 8 Data of mouse Mitf qPCR (FC). (XLSX 27 kb)

Microphthalmia-associated transcription factor

Expression (computer science)

10.6084/m9.figshare.c.3628799_d3

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Citations (0)

Comparative analysis of the pig BAC sequence involved in the regulation of myostatin gene

Science in China Series C Life Sciences (2005)

Zhengquan Yu Yan Li Qingyong Meng Jing Yuan Zhihui Zhao

Myostatin

TATA box

CAAT box

Transcription

10.1007/bf02879670

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Citations (8)

Nfatc1⁺ colonic stem cells contribute to regeneration upon colitis

Journal of Gastroenterology and Hepatology (2022)

Jianyang Wang Linkuo Shang Jiahui Zhang Zhengquan Yu Jiaqiang Huang

Colonic stem cells play important roles in both normal epithelial turnover and injury repair. Lgr5+ colonic stem cells are highly susceptible to DSS-induced damage. However, it is still unclear how colonic stem cells regenerate injured epithelium during colitis. Here, we explored the functions of a new population of NFATc1+ colonic stem cells in experimental colitis.Nfatc1+ colonic stem cells were labeled using Nfatc1CreERT2 ;R26mTmG reporter mice. Immunostaining assays were used to detect Goblet cells, enteroendocrine cells, and intestinal stem/progenitor cells. We performed lineage tracing assay to investigate whether Nfatc1+ cells are real colonic stem cells using Nfatc1CreERT2 ;R26mTmG mice. The contribution of Nfatc1+ stem cells on epithelial regeneration was detected in experimental colitis induced by DSS.Nfatc1-reporter marked cells are enriched for +3 to +5 position in colonic crypts, and they are overlapped with Sox9+ cells and Hopx+ cells that have been identified as stem cells in small intestine. However, Nfatc1-reporter marked cells are not overlapped with Lgr5+ colonic stem cells, as well as differentiated goblet cells and enteroendocrine cells. Furthermore, Nfatc1-reporter marked cells are able to give rise to all lineages of the colonic epithelium, and they preferentially contribute to the regeneration of colonic epithelium in DSS-induced experimental colitis.Nfatc1+ cells were identified as a novel population of colonic stem cells that are primarily located at +3 to +5 position and contribute to epithelial regeneration during colitis.

LGR5

Amniotic epithelial cells

Intestinal epithelium

Amniotic stem cells

10.1111/jgh.15790

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Citations (2)

Musashi proteins are post-transcriptional regulators of the epithelial-luminal cell state

eLife (2014)

Yarden Katz Feifei Li Nicole Lambert Ethan S. Sokol Wai Leong Tam

The conserved Musashi (Msi) family of RNA binding proteins are expressed in stem/progenitor and cancer cells, but generally absent from differentiated cells, consistent with a role in cell state regulation. We found that Msi genes are rarely mutated but frequently overexpressed in human cancers and are associated with an epithelial-luminal cell state. Using ribosome profiling and RNA-seq analysis, we found that Msi proteins regulate translation of genes implicated in epithelial cell biology and epithelial-to-mesenchymal transition (EMT), and promote an epithelial splicing pattern. Overexpression of Msi proteins inhibited the translation of Jagged1, a factor required for EMT, and repressed EMT in cell culture and in mammary gland in vivo. Knockdown of Msis in epithelial cancer cells promoted loss of epithelial identity. Our results show that mammalian Msi proteins contribute to an epithelial gene expression program in neural and mammary cell types.

10.7554/elife.03915

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Citations (87)

SELENOI Functions as a Key Modulator of Ferroptosis Pathway in Colitis and Colorectal Cancer

Advanced Science (2024)

Xin Huang Yang Xu M. Zhang Tong Li Kongdi Zhu

Ferroptosis plays important roles both in normal physiology and multiple human diseases. It is well known that selenoprotein named glutathione peroxidase 4 (GPX4) is a crucial regulator for ferroptosis. However, it remains unknown whether other selenoproteins responsible for the regulation of ferroptosis, particularly in gut diseases. In this study, it is observed that Selenoprotein I (Selenoi) prevents ferroptosis by maintaining ether lipids homeostasis. Specific deletion of Selenoi in intestinal epithelial cells induced the occurrence of ferroptosis, leading to impaired intestinal regeneration and compromised colonic tumor growth. Mechanistically, Selenoi deficiency causes a remarkable decrease in ether-linked phosphatidylethanolamine (ePE) and a marked increase in ether-linked phosphatidylcholine (ePC). The imbalance of ePE and ePC results in the upregulation of phospholipase A2, group IIA (Pla2g2a) and group V (Pla2g5), as well as arachidonate-15-lipoxygenase (Alox15), which give rise to excessive lipid peroxidation. Knockdown of PLA2G2A, PLA2G5, or ALOX15 can reverse the ferroptosis phenotypes, suggesting that they are downstream effectors of SELENOI. Strikingly, GPX4 overexpression cannot rescue the ferroptosis phenotypes of SELENOI-knockdown cells, while SELENOI overexpression can partially rescue GPX4-knockdown-induced ferroptosis. It suggests that SELENOI prevents ferroptosis independent of GPX4. Taken together, these findings strongly support the notion that SELENOI functions as a novel suppressor of ferroptosis during colitis and colon tumorigenesis.

GPX4

Selenoprotein

10.1002/advs.202404073

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Citations (10)

The Msi Family of RNA-Binding Proteins Function Redundantly as Intestinal Oncoproteins

Cell Reports (2015)

Ning Li Maryam Yousefi Angela Nakauka‐Ddamba Fan Li Lee E. Vandivier

Members of the Msi family of RNA-binding proteins have recently emerged as potent oncoproteins in a range of malignancies. MSI2 is highly expressed in hematopoietic cancers, where it is required for disease maintenance. In contrast to the hematopoietic system, colorectal cancers can express both Msi family members, MSI1 and MSI2. Here, we demonstrate that, in the intestinal epithelium, Msi1 and Msi2 have analogous oncogenic effects. Further, comparison of Msi1/2-induced gene expression programs and transcriptome-wide analyses of Msi1/2-RNA-binding targets reveal significant functional overlap, including induction of the PDK-Akt-mTORC1 axis. Ultimately, we demonstrate that concomitant loss of function of both MSI family members is sufficient to abrogate the growth of human colorectal cancer cells, and Msi gene deletion inhibits tumorigenesis in several mouse models of intestinal cancer. Our findings demonstrate that MSI1 and MSI2 act as functionally redundant oncoproteins required for the ontogeny of intestinal cancers.

10.1016/j.celrep.2015.11.022

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Citations (91)

Microsurgical treatment of intracranial thrombotic giant aneurysms( report of 11 cases)

Yabo Huang Shiming Zhang Zhong Wang Zhengquan Yu Gang Cui

Objective To study the clinical features and surgical management of intracranial thrombotic giant aneurysms.Methods A retrospective study was performed for 11 patients with intracranial thrombotic giant aneurysms.The clinical presentation, clinical classification, surgical approaches and therapeutic efficacy were reviewed.Results The treatment included thrombectomy - aneurysm clip reconstruction in 9 cases, thrombectomy - aneurysm isolate in 1, and cervical internal carotid artery ligation in 1.The postoperative DSA or CTA showed that complete angiographic obliteration was achieved in 10 cases.Follow - up period was from 3 months to 6 months, the clinical outcomes of these patients were evaluated by Glasgow Outcome Scale grades.GOS of 8 cases were improved.There were minor deficit in 1 case, major deficit in 1 and one death.Conclusions The surgical treatment for intracranial thrombotic giant aneurysms is very difficult.It is a good method to occlude the parent artery temporally, eliminate intraaneurysmal thrombus and reconstruct parent artery.Intraoperative microvascular Doppler sonography (MVD) monitoring is helpful. Key words: Intracranial aneurysm; Thrombus; Microsurgical clipping; Thrombectomy

Clipping (morphology)

Presentation (obstetrics)

10.3760/cma.j.issn.1001-2346.2011.08.015

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Hormone-Responsive BMP Signaling Expands Myoepithelial Cell Lineages and Prevents Alveolar Precocity in Mammary Gland

Frontiers in Cell and Developmental Biology (2021)

Chunlei Shao Pengbo Lou Ruiqi Liu Xueyun Bi Guilin Li

Myoepithelial and luminal cells synergistically expand in the mammary gland during pregnancy, and this process is precisely governed by hormone-related signaling pathways. The bone morphogenetic protein (BMP) signaling pathway is now known to play crucial roles in all organ systems. However, the functions of BMP signaling in the mammary gland remain unclear. Here, we found that BMPR1a is upregulated by hormone-induced Sp1 at pregnancy. Using a doxycycline (Dox)-inducible BMPR1a conditional knockout mouse model, we demonstrated that loss of BMPR1a in myoepithelium results in compromised myoepithelial integrity, reduced mammary stem cells and precocious alveolar differentiation during pregnancy. Mechanistically, BMPR1a regulates the expression of p63 and Slug, two key regulators of myoepithelial maintenance, through pSmad1/5-Smad4 complexes, and consequently activate P-cadherin during pregnancy. Furthermore, we observed that loss of BMPR1a in myoepithelium results in the upregulation of a secreted protein Spp1 that could account for the precocious alveolar differentiation in luminal layer, suggesting a defective basal-to-luminal paracrine signaling mechanism. Collectively, these findings identify a novel role of BMP signaling in maintaining the identity of myoepithelial cells and suppressing precocious alveolar formation.

Conditional gene knockout

10.3389/fcell.2021.691050

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Citations (6)