Motivated forgetting is a psychological defense mechanism whereby people cope with threatening and unwanted memories by suppressing them from consciousness. A series of laboratory experiments investigate whether social identity threat can motivate people subsequently to forget identity-linked marketing promotions. To this effect, whereas social identity priming improves memory for identity-linked promotions, priming coupled with social identity threat (i.e., negative identity-related feedback) impairs memory. Importantly, this identity threat effect occurs only among people who identify strongly with their in-group and only for explicit memory. Implicit memory, in contrast, remains intact under threat. Additionally, the identity threat effect is eliminated (i.e., explicit memory is restored) if people affirm the threatened social identity, thereby mitigating the threat, prior to memory retrieval. Finally, the identity threat effect occurs only when automatic processes guide forgetting. When forgetting is guided by deliberate and controlled processes, the tobe-forgotten memories intrude into consciousness.
Periodontitis is a highly prevalent infectious disease associated genetically with coronary heart disease (CHD). The effects of proprotein convertase subtilisin/kexin type 9 (PCSK9), a critical regulator of CHD, on periodontitis have not been studied to date. Here, we found that PCSK9 expression was increased in periodontitis patients and Porphyromonas gingivalis (Pg)-infected mice. Loss of PCSK9 attenuated Pg-induced periodontal bone loss in mice. First, PCSK9 deficiency reduced the release of inflammation-associated cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukin 1β, in vitro and in vivo. Second, its deficiency enhanced Pg and endotoxin clearance during Pg invasion in part by upregulating CD36 and low-density lipoprotein receptor (LDLR), respectively. However, after berberine treatment, periodontal bone regeneration in the PCSK9 knockout group was significantly lower than that in wild-type. This was because PCSK9 overexpression promoted osteogenic differentiation of periodontal ligament stem cells (PDLCs) prechallenged by TNF-α. Furthermore, PCSK9 could rescue PDLC osteogenesis by repressing the NF-κB signaling pathway by interacting with TRAF2. These results suggest that PCSK9 may be a potent drug target for treating periodontitis.
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