A Preliminary Study Of Interleukin-8and Its Receptor’s Experssion、Regulation In The Dental Pulp Stem Cell

The dental pulp tissue is a highly differentiated mesenchymal tissue characterized bythe presence of odontoblasts and it is surrounded by a rigid mineralized tissue.The dentalpulp tissue filled with blood vessels and nerve bundles emanating from the apical region.Mechanical、chemical、thermal、microbial irritants and other stimulation activate varioustypes of inflammatory responses, involving vascular、 lymphatic and local tissuereactions,thereby causing the pulp tissue degeneration and necrosis.The pulp tissue has aimportant role to the internal environment of the tooth，meanwhile it is a essential elementof long-term retention of teeth.Like other connective tissue pulp tissue has the ability toself-regeneration,stem cell are able to ensure that tissue repair and regeneration.Thedental pulp stem cells（DPSCs） laocated at dental pulp tissue,which has a strongproliferation and differentiation capacity.DPSCs were thought to possess a potent capacityto differentiate into odontoblasts、osteoblastic、neuronic and adipocytic cell type in vitro[1].Many research reports that DPSCs can migration into injured site[2,3].So DPSCs isessential for pulp injured repair.Recent study found that chemokines can promoterecruitment DPSCs to injured site and differentiate into odontoblasts.These odontoblastsinvolved into the repair of injury pulp tissue.It can be inferred that the activation andmigration of DPSCs is essential for the repair of injury pulp. Some research found thatinjured odontoblasts and vascular tissue can recruitment DPSCs into the injured site[2,3].IL-8（Interleukin-8，IL-8）, as a member of the CXC chemokine family ofcytokines,has been proved to be one of major mediators of inflammation that contributesto sequestration of neutrophils at injured sites of tissue[4],meanwhile vitro experimentsshowed that IL-8can promote the ability of angiogenesis of epithelial cells.IL-8isconsidered to be a vascular-derived proinflammatory chemokines, recent studies havefound that IL-8has the ability to recruitment tissue stem cells to the injured site[6,7]. IL-8is not only expressed in healthy human pulps but also be detected a high expression ofIL-8in inflammatory tissues,the study found that IL-8can be detected a low expression inthe healthy pulp tissue and pulp tissue exudate,but there is a high expression of IL-8in theinflammatory tissues.In the chronic pulpitis pulp tissue the content of IL-8is about5timeshigher than normal tissue,but in acute pulpitis pulp tissue the content of IL-8is about10times higher than normal tissue[8].The current study found that there are at least two types of IL-8R (Interleukin-8receptor, IL-8R), which mainly distributed in the surface of neutrophils[9],typeⅠreceptor（CXCR-1） can specific combine with IL-8,type Ⅱ receptor（CXCR-2）except cancombine with IL-8but also can combine with growth-regulated oncogene（GRO）、monocyte inflammatory protein-2（MIP-2）and so on.The current study has shown that pro-inflammatory cytokines can stimulate DPSCssecrete IL-8,meanwhile IL-8R can be detect on the cytomembrane of DPSCs,but does notexplicitly found there is receptor CXCR-1or CXCR-2.This experiment will study the cellsurface expression of CXCR1on human dental pulp stem cells(hDPSCs) in vitro, then usedifferent concentrations of IL-8stimulation hDPSCs and observe the changes in the ability of the proliferation and migration of hDPSCs.And then study whether IL-8/CXCR-1pathway play an important role in recruitment hDPSCSs to injured site.Result：CXCR-1was expressed in cytomembrane of hDPCSs．In addition，IL-8increased the chemotactic migration of hDPSCs significantly after4h’s incubation withthe concentrations of200ng/mL、500ng/mL (P <0．05）；IL-8stimulated the hDPSCsproliferation at the concentrations of10ng/mL、50ng/mL、100ng/mL after48h’sincubation(P <0.05）．Conclusions：IL-8accelerated the migration and the proliferation of hDPSCs whichexpressed CXCR-1．IL-8/CXCR-1pathway may be play an important role to promoterecruitment of hDPSCs to the injured site．...