Mechanical Stress Activates Proinflammatory Cytokines and Antioxidant Defense Enzymes in Human Dental Pulp Cells

The role of heme oxygenase-1 in mechanical stress- and lipopolysaccharide-induced osteogenic differentiation in human periodontal ligament cells

“…[19][20][21][22][23][24] In the present study, we found that MS increased HO-1 mRNA and protein expression in PDLCs. These findings are consistent with our previous study in which osteogenic differentiation Figure 4.…”

“…Previously, we reported that the HO-1 pathway is a key mechanism for the adaptation to stressful conditions and the recovery from injurious events by dental cells. [19][20][21][22][23][24] Moreover, the expression of HO-1 is related to adipogenesis by human MSCs, 25 osteoblastic differentiation by PDLCs 23 and neuronal differentiation by MSCs. 26 Because HO-1 is associated with differentiation, it is plausible to postulate that HO-1 is involved in the response of PDLCs to MS and bacterial infection as well as in the differentiation of PDLCs to osteoblast-like cells.…”

Anti-inflammatory effects of apigenin on nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via heme oxygenase-1

“…Previously, we reported that the HO-1 pathway is a key mechanism for both the adaptation of cells to stressful conditions and their recovery from injurious events in human pulp and PDL cells [27][28][29][30][31][32]. Moreover, HO-1 has therapeutic potential in hepatoprotection [33], inflammatory arthritis [34], psoriasiform skin lesions [35], neuroinflammation [36], inflammatory bowel disease [37], and periodontitis [15].…”

Prostaglandin F2α-Induced Interleukin-8 Production in Human Dental Pulp Cells Is Associated With MEK/ERK Signaling

“…It consists of an odontoblast layer adjacent to the dentin and an immunocompetent tissue containing pulp cells, extracellular matrix, nerves, and vascular elements (2). When exposed to mechanical injury or direct invasion by microorganisms and their metabolic products, pulpal inflammation and even necrosis are often noted (3,4). A number of chemical factors such as cytokines, chemokines, substance P, and prostaglandins (PGs) are suggested to mediate pulpal inflammation (5)(6)(7).…”