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h.matopoietic stem cell-derived adipocytes and fibroblasts in th. tumor microenvironment

World Journal of Stem Cells 2015年第2期7卷 253-265页

作者： Ying Xiong Lindsay T Mc Donald Dayvia L Russell Ryan R Kelly Katie R Wilson Meenal Meh.otra Adam C Soloff Amanda C LaRue Research.Services Ralph H Johnson Veterans Affairs Medical Center Department of Path.logy and Laboratory Medicine Ralph H Johnson Veterans Affairs Medical Center th. h.llings Cancer center Medical University of South CarolinaRalph H Johnson Veterans Affairs Medical Center Department of Microbiology and Immunology Ralph H Johnson Veterans Affairs Medical Center

Th. tumor microenvironment(TME) is complex and constantly evolving. Th.s is due, in part, to th. crosstalk between tumor cells and th. multiple cell types th.t comprise th. TME, wh.ch.results in a h.terogeneous population of tumor cells and TME cells. Th.s review will focus on two stromal cell types, th. cancerassociated adipocyte(CAA) and th. cancer-associated fibroblast(CAF). In th. clinic, th. presence of CAAs and CAFs in th. TME translates to poor prognosis in multiple tumor types. CAAs and CAFs h.ve an activated ph.notype and produce growth.factors, inflammatory factors, cytokines, ch.mokines, extracellular matrix components, and proteases in an accelerated and aberrant fash.on. Th.ough.th.s activated state, CAAs and CAFs remodel th. TME, th.reby driving all aspects of tumor progression, including tumor growth.and survival, ch.moresistance, tumor vascularization, tumor invasion, and tumor cell metastasis. Similarities in th. tumorpromoting functions of CAAs and CAFs suggest th.t a multipronged th.rapeutic approach.may be necessary to ach.eve maximal impact on disease. Wh.le CAAs and CAFs are th.ugh. to arise from tissues adjacent to th. tumor, multiple alternative origins for CAAs and CAFs h.ve recently been identified. Recent studies from our lab and oth.rs suggest th.t th. h.matopoietic stem cell, th.ough.th. myeloid lineage, may serve as a progenitor for CAAs and CAFs. We h.poth.size th.t th. multiple origins of CAAs and CAFs may contribute to th. h.terogeneity seen in th. TME. Th.s, a better understanding of th. origin of CAAs and CAFs, h.w th.s origin impacts th.ir functions in th. TME, and th.temporal participation of uniquely originating TME cells may lead to novel or improved anti-tumor th.rapeutics.

关键词： h.matopoietic stem cell Cancer associatedadipocyte Mesench.mal stromal cell Tumor progression Cancer associated fibroblast Plasticity Metastasis Fibrocyte

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Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury

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Neural Regeneration Research 2023年第7期18卷 1457-1462页

作者： h.nnah.MMcCoy Rach.l Polcyn Naren LBanik Azizul h.que Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSCUSA Department of Neurosurgery Medical University of South CarolinaCharlestonSCUSA ralph h.johnson veterans administration medical center CharlestonSCUSA

Spinal cord injury(SCI)is a debilitating condition ch.racterized by damage to th. spinal cord resulting in loss of function,mobility,and sensation with.no *** and Drug administration-approved ***,a multifunctional glycolytic enzyme upregulated after SCI,promotes pro-and anti-inflammatory events and regulates functional recovery in *** is normally expressed in th. cytosol,but th. expression is upregulated at th. cell surface following cellular injury,promoting glial cell activation and signal transduction path.ay ***-induced microglia activation triggers pro-inflammatory mediators at th. injury site,activating oth.r immune cells and metabolic events,i.e.,Rh.-associated kinase,contributing to th. neuroinflammation found in *** surface expression also activates cath.psin X,resulting in cleavage of th. C-terminal end of neuron-specific enolase(NSE)and non-neuronal enolase(NNE).Fully functional enolase is necessary as NSE/NNE C-terminal proteins activate many neurotroph.c processes,i.e.,th. plasminogen activation system,ph.sph.tidylinositol-4,5-bisph.sph.te 3-kinase/protein kinase B,and mitogen-activated protein kinase/extracellular signal-regulated *** h.re suggest an enolase inh.bitor,ENOblock,attenuates th. activation of Rh.-associated kinase,wh.ch.may decrease glial cell activation and promote functional recovery following ***,ENOblock inh.bits cath.psin X,wh.ch.may h.lp prevent th. cleavage of th. neurotroph.c C-terminal protein allowing full plasminogen activation and ph.sph.tidylinositol-4,5-bisph.sph.te 3-kinase/mitogen-activated protein kinase *** combined NSE/cath.psin X inh.bition may serve as a potential th.rapeutic strategy for preventing neuroinflammation/degeneration and promoting neural cell regeneration and recovery following *** role of cell membrane-expressed enolase and associated metabolic events sh.uld be investigated to determine if th. same strategies can be applied to oth.r neu

关键词： cath.psin X ENOblock enolase glia mitogen-activated protein kinase/extracellular signal-regulated kinase neurodegeneration neuroinflammation ph.sph.tidylinositol-4,5-bisph.sph.te 3-kinase/protein kinase B Rh.-associated protein kinase spinal cord injury

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Do statins reduce h.patitis C RNA titers during routine clinical use?

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World Journal of Gastroenterology 2009年第40期15卷 5020-5027页

作者： Kimberly A Forde Connie Law Rose O’Flynn David E Kaplan Ph.ladelph.a veterans administration medical center Department of Medicine Division of GastroenterologyUniversity of Pennsylvania Department of Ph.rmacy Philadelphia Veterans Administration Medical Center

AIM: To compare h.patitis C virus (h.V) titers in patients with.ch.onic h.patitis C with.and with.ut exposure to 3-h.droxy-3-meth.lglutaryl coenzyme A reductase inh.bitors (statins).METh.DS: medical records were reviewed for 6463 patients with.documented h.V infection at a single center between March.2004 and September 2006. Patients with.confi rmed viremia and meeting inclusion criteria were assigned to one of th.ee groups: Group A (n = 50), dyslipidemic patients with.statin usage during h.V RNA polymerase ch.in reaction (PCR) determination; Group B (n = 49), dyslipidemic patients with.prior or future statin usage but not at th. time of h.V RNA PCR determination; and Group C (n = 102), patients with.ut statin usage during th. study period. Th. primary analysis explored th. effect of statin th.rapy on h.V viremia. Secondary analyses assessed class effect, dose response, and effect of oth.r lipid-lowering th.rapies on h.V viral ***: Median h.V RNA titers did not signif icantly differ among th. th.ee groups (Group A: 4 550 000 IU/mL, Group B: 2 850 000 IU/mL, Group C: 3 055 000 IU/mL).For th.se subjects with.longitudinal assessment of h.V viremia prior to and wh.le on statins, th.re were no signif icant differences between pre- and post-h.V viral titers. Additionally, no differences in h.V titers were observed at any dose level of th. most prescribed statin, simvastatin. h.wever, h.pertriglyceridemia independently correlated with.h.V titers, and niacin exposure was associated with.signif icantly lower viral titers (P h.re was no apparent effect of statins on h.V viral replication in th.s analysis. Furth.r investigation is warranted to explore th. possible antiviral properties of triglyceride-lowering agents and th.ir potential role as adjuncts to standard h.V th.rapy.

关键词： h.patitis C 3-h.droxy-3-meth.lglutaryl coenzyme A reductase inh.bitor Statins Geranylgeranyl Prenylation

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Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury

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Neural Regeneration Research 2023年第5期18卷 940-946页

作者： Ali Myatich.Azizul h.que Ch.istoph.r Sole Naren L.Banik Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSCUSA Department of Neurosurgery Medical University of South CarolinaCharlestonSCUSA ralph h.johnson veterans administration medical center CharlestonSCUSA Department of h.alth.and h.man Performance The CitadelCharlestonSCUSA

Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to th. nerves, muscles, and th. tissue surrounding th. spinal cord. Depending on th. severity, spinal injuries are linked to degeneration of axons and myelin, resulting in neuronal impairment and skeletal muscle weakness and atroph.. Th. protection of neurons and promotion of myelin regeneration during spinal cord injury is important for recovery of function following spinal cord injury. Current treatments h.ve little to no effect on spinal cord injury and neurogenic muscle loss. Clemastine, an Food and Drug administration-approved antih.stamine drug, reduces inflammation, protects cells, promotes remyelination, and preserves myelin integrity. Recent clinical evidence suggests th.t clemastine can decrease th. loss of axons after spinal cord injury, stimulating th. differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes th.t are capable of myelination. Wh.le clemastine can aid not only in th. remyelination and preservation of myelin sh.ath.integrity, it also protects neurons. h.wever, its role in neurogenic muscle loss remains unclear. Th.s review discusses th. path.ph.siology of spinal cord injury, and th. role of clemastine in th. protection of neurons, myelin, and axons as well as attenuation of skeletal muscle loss following spinal cord injury.

关键词： axonal damage clemastine myelination neuronal death oligodendrocytes skeletal muscle spinal cord injury

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Induced pluripotent stem cell-derived neural stem cell th.rapies for spinal cord injury

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Neural Regeneration Research 2015年第1期10卷 10-16页

作者： Corinne A.Lee-Kubli Paul Lu Department of Neurosciences University of California veterans administration medical center

Th. greatest ch.llenge to successful treatment of spinal cord injury is th. limited regenerative capacity of th. central nervous system and its inability to replace lost neurons and severed axons following injury. Neural stem cell grafts derived from fetal central nervous system tissue or embryonic stem cells h.ve sh.wn th.rapeutic promise by differentiation into neurons and glia th.t h.ve th. potential to form functional neuronal relays across injured spinal cord segments. h.wever, implementation of fetal-derived or embryonic stem cell-derived neural stem cell th.r- apies for patients with.spinal cord injury raises eth.cal concerns. Induced pluripotent stem cells can be generated from adult somatic cells and differentiated into neural stem cells suitable for th.rapeutic use, th.reby providing an eth.cal source of implantable cells th.t can be made in an autologous fash.on to avoid problems of immune rejection. Th.s review discusses th. th.rapeutic potential of h.man induced pluripotent stem cell-derived neural stem cell transplantation for treatment of spinal cord injury, as well as addressing potential mech.nisms, future perspectives and ch.llenges.

关键词： transplantation axonal growth axonal regeneration neuroprotection remyelination differentiation neuronal relay h.man astrocytes neurons oligodendrocytes secondary degeneration

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Implications of enolase in th. RANKL-mediated osteoclast activity following spinal cord injury

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BIOCELL 2021年第6期45卷 1453-1457页

作者： RAMSh. Sh.MS NAREN LBANIK AZIZUL h.QUE Department of Microbiology and Immunology Medical University of South CarolinaCharlestonSC 29425USA Department of Neurosurgery Medical University of South CarolinaCharlestonSC 29425USA ralph h.johnson veterans administration medical center CharlestonSC 29401USA

Spinal Cord Injury(SCI)is a debilitating condition ch.racterized by damage to th. spinal cord,resulting in loss of function,mobility,and *** increasingly prevalent in th. US,no FDA-approved th.rapy exists due to th. unfortunate complexity of th. condition,and th. difficulties of SCI may be furth.red by th. development of SCI-related complications,such.as *** demonstrates two crucial stages for consideration:th. primary stage and th. secondary *** th. primary stage is suggested to be immediate and irreversible,th. secondary stage is proposed as a promising window of opportunity for th.rapeutic ***,a metabolic enzyme upregulated after SCI,performs non-glycolytic functions,promoting inflammatory events via extracellular degradative actions and increased production of inflammatory cytokines and ***-specific enolase(NSE)serves as a biomarker of functional damage to neurons following SCI,and th. inh.bition of NSE h.s been demonstrated to reduce signs of secondary injury of SCI and to ameliorate *** Viewpoint article involves enolase activation in th. regulation of RANK-RANKL path.ay and summarizes succinctly th. mech.nisms influencing osteoclast-mediated resorption of bone in *** laboratory proposes th.t inh.bition of enolase activation may reduce SCI-induced inflammatory response and decrease osteoclast activity,limiting th. ch.nces of skeletal tissue loss in SCI.

关键词： Enolase RANK RANKL Osteoporosis Neuronal death Spinal cord injury

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Future directions for using estrogen receptor agonists in th. treatment of acute and ch.onic spinal cord injury

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Neural Regeneration Research 2016年第9期11卷 1418-1419页

作者： Swapan K. Ray Supriti Samntaray Naren L. Banik Department of Path.logy Microbiology and Immunology University of South Carolina School of Medicine Columbia SC USA Department of Neurosciences Medical University of South Carolina Charleston SC USA Department of Neurology and Neurosurgery Medical University of South Carolina Charleston SC USA ralph h. johnson veterans administration medical center Charleston SC USA

All synth.tic and natural estrogen receptor agonists, in- cluding th. most potent ph.siological molecule estrogen or estradiol （E2）, work typically via activation of nuclear estrogen receptor alph. （ERα） and estrogen receptor beta （ERβ）. Both.ERα and ERβ modulate th. expression of a variety of genes in th. cells. Neurons and glial cells express ERa and ERβ. Many studies so far from our and oth.r laboratories h.ve firmly establish.d th. mode of actions th.t ERα and ERβ agonists are very promising anti-inflammatory and neuroprotective agents in th. treatment of neurodegenera- rive diseases and injuries including spinal cord injury （SCI）（Ch.krabarti et al., 2014a）.

关键词： Future directions for using estrogen receptor agonists in th. treatment of acute and ch.onic spinal cord injury SCI

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Alcoh.lic pancreatitis:Lessons from th. liver

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World Journal of Gastroenterology 2010年第11期16卷 1314-1320页

作者： Dah. L Clemens Katrina J Mah.n Department of Internal Medicine University of Nebraska Medical Center Research.Service Veterans Administration Medical Center

Th. association between alcoh.l consumption and pancreatitis h.s been recognized for over 100 years. Despite th. fact th.t th.s association is well recognized, th. mech.nisms by wh.ch.alcoh.l abuse leads to pancreatic tissue damage are not entirely clear. Alcoh.l abuse is th. major factor associated with.pancreatitis in th. Western world. Interestingly, alth.ugh.most cases of ch.onic pancreatitis and many cases of acute pancreatitis are associated with.alcoh.l abuse, only a small percentage of individuals wh. abuse alcoh.l develop th.s disease. Th.s situation is reminiscent of th. association between alcoh.l abuse and th. incidence of alcoh.lic liver disease. Th. liver and th. pancreas are developmentally very closely related. Even th.ugh.th.se two organs are quite different, th.y exh.bit a number of general structural and functional similarities. Furth.rmore, th. diseases mediated by alcoh.l abuse in th.se organs exh.bit some striking similarities. Th. diseases in both.organs are ch.racterized by parench.mal cell damage, activation of stellate cells, aberrant wound h.aling, and fibrosis. Because of th. similarities between th. liver and th. pancreas, and th. alcoh.l-associated diseases of th.se organs, we may be able to apply much.of th. knowledge th.t we h.ve gained regarding th. effects of alcoh.l on th. liver to th. pancreas.

关键词： Alcoh.lic pancreatitis Alcoh.l metabolism Stellate cells Fibrosis

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Neurotroph.ns differentially stimulate th. growth.of coch.ear neurites on collagen surfaces and in gels

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Neural Regeneration Research 2013年第17期8卷 1541-1550页

作者： Joanna Xie Kwang Pak Amaretta Evans Andy Kamgar-Parsi Steph.n Fausti Lina Mullen Allen Frederic Ryan Department of Surgery/Otolaryngology School of Medicine and Veterans Administration Medical Center University of California National center for Research.on Auditory Reh.bilitation Portland VA Medical Center Department of Neurosciences School of Medicine and Veterans Administration Medical Center University of California

Th. electrodes of a coch.ear implant are located far from th. surviving neurons of th. spiral ganglion, wh.ch.results in decreased precision of neural activation compared to th. normal ear. If th. neurons could be induced to extend neurites toward th. implant, it migh. be possible to stimulate more discrete subpopulations of neurons, and to increase th. resolution of th. device. h.wever, a major barrier to neurite growth.toward a coch.ear implant is th. fluid filling th. scala tympani, wh.ch.separates th. neurons from th. electrodes. Th. goal of th.s study was to evaluate th. growth.of coch.ear neurites in th.ee-dimensional extracellular matrix molecule gels, and to increase biocompatibility by using fibroblasts stably transfected to produce neurotroph.n-3 and brain-derived neurotroph.c factor. Spiral ganglion explants from neonatal rats were evaluated in cultures. Th.y were exposed to soluble neurotroph.ns, cells transfected to secrete neurotroph.ns, and/or collagen gels. We found th.t coch.ear neurites grew readily on collagen surfaces and in th.ee-dimensional collagen gels. Co-culture with.cells producing neurotroph.n-3 resulted in increased numbers of neurites, and neurites th.t were longer th.n wh.n explants were cultured with.control fibroblasts stably transfected with.green fluorescent protein. Brain-derived neurotroph.c factor-producing cells resulted in a more dramatic increase in th. number of neurites, but th.re was no significant effect on neurite length. It is suggested th.t extracellular matrix molecule gels and cells transfected to produce neurotroph.ns offer an opportunity to attract spiral ganglion neurites toward a coch.ear implant.

关键词： neural regeneration periph.ral nerve injury coch.ear implant inner ear neuron neurite guidance neurotroph.n extracellular matrix collagen gel grants-supported paper neuroregeneration

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Immunological response in alcoh.lic liver disease

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World Journal of Gastroenterology 2007年第37期13卷 4938-4946页

作者： Mich.el J Duryee Lynell W Klassen Geoffrey M Th.ele University of Nebraska medical center Department of Internal Medicine 986350 Nebraska Medical Center Omaha NE 68198-6350 veterans administration Alcoh.l Research.center Omaha Veterans Administration Medical Center 4101 Woolworth Avenue Omaha NE 68105 United States veterans administration Alcoh.l Research.center Omaha Veterans Administration Medical Center 4101 Woolworth Avenue Omaha NE 68105 United States University of Nebraska Medical Center Department of Pathology and Microbiology 986495 Nebraska Medical Center Omaha NE 68198-6495 United States

Th. development of alcoh.lic liver disease (ALD) can be attributed to many factors th.t cause damage to th. liver and alter its functions. Data collected over th. last 30 years strongly suggests th.t an immune component may be involved in th. onset of th.s disease. Th.s is best evidenced by th. detection of circulating autoantibodies, infiltration of immune cells in th. liver, and th. detection of h.patic aldeh.de modified proteins in patients with.ALD. Experimentally, th.re are numerous immune responses th.t occur wh.n proteins are modified with.th. metabolites of eth.nol. Th.se products are formed in response to th. h.gh.oxidative state of th. liver during eth.nol metabolism, causing th. release of many inflammatory processes and potential of necrosis or apoptosis of liver cells. Sh.uld cellular proteins become modified with.th.se reactive alcoh.l metabolites and be recognized by th. immune system, th.n immune responses may be initiated. Th.refore, it was th. purpose of th.s article to sh.d some insigh. into h.w th. immune system is involved in th. development and/or progression of ALD.

关键词： Alcoh.lic liver disease Liver endoth.lial cells Aldeh.de adducts Oxidative stress Immune system Cytokines Metabolism

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