Airway Epithelial Cell Migration Dynamics: Mmp-9 Role in Cell–Extracellular Matrix Remodeling

Cell spreading and migration associated with the expression of the 92-kD gelatinase (matrix metalloproteinase 9 or MMP-9) are important mechanisms involved in the repair of the respiratory epithelium. We investigated the location of MMP-9 and its potential role in migrating human bronchial epithelial cells (HBEC). In vivo and in vitro, MMP-9 accumulated in migrating HBEC located at the leading edge of a wound and MMP-9 expression paralleled cell migration speed. MMP-9 accumulated through an actin-dependent pathway in the advancing lamellipodia of migrating cells and was subsequently found active in the extracellular matrix (ECM). Lamellipodia became anchored through primordial contacts established with type IV collagen. MMP-9 became amassed behind collagen IV where there were fewer cell–ECM contacts. Both collagen IV and MMP-9 were involved in cell migration because when cell–collagen IV interaction was blocked, cells spread slightly but did not migrate; and when MMP-9 activation was prevented, cells remained fixed on primordial contacts and did not advance at all. These observations suggest that MMP-9 controls the migration of repairing HBEC by remodeling the provisional ECM implicated in primordial contacts

SJS/TEN 2019: From science to translation.

Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) are potentially life-threatening, immune-mediated adverse reactions characterized by widespread erythema, epidermal necrosis, and detachment of skin and mucosa. Efforts to grow and develop functional international collaborations and a multidisciplinary interactive network focusing on SJS/TEN as an uncommon but high burden disease will be necessary to improve efforts in prevention, early diagnosis and improved acute and long-term management. SJS/TEN 2019: From Science to Translation was a 1.5-day scientific program held April 26-27, 2019, in Vancouver, Canada. The meeting successfully engaged clinicians, researchers, and patients and conducted many productive discussions on research and patient care needs

Syllable Weakening in Kagoshima Japanese An Element-Based Analysis

This paper examines syllable weakening or nisshōka (入声化) in Kagoshima Japanese (KJ), where high vowel apocope feeds lenition, leading to correspondences such as Tōkyō Japanese (TJ) [kaki] ‘persimmon’ and Kagoshima [kaʔ]. The traditional pattern noted in the literature is quite clear. Apocope elides stem-final /u/ or /i/. The preceding onset is lenited in one of four ways: 1) stops and affricates are debuccalised (/kaki/ > [kaʔ] ‘persimmon’); 2) fricatives undergo voicing neutralisation (TJ [kazu] > KJ [kas] ‘number’); 3) nasals undergo place loss (TJ [kami] > KJ [kaɴ] ‘paper’); 4) rhotics undergo gliding (TJ [maru] > [maj] ‘round’). This paper presents an initial analysis of the data within Element Theory representational framework

Activation of Mitogen Activated Protein Kinase pathways during the death of PC12 cells is dependent on the state of differentiation

PC12 cells that are differentiated with NGF and cAMP become totally dependent on these factors for their survival, unlike those that are differentiated with NGF alone. We have asked whether the MAP Kinases, ERKs, JNKs and p38s play a role in the cell death induced by withdrawal of trophic factors on NGF- and NGF/cAMP-differentiated PC12 cells. By Western-blot analyses with antibodies directed against the activated forms of these kinases, we show that when the trophic factors were withdrawn, ERK phosphorylation was reduced to very low levels within 1 h in both cases. Changes in the other enzymes were observed only in the NGF/cAMP-differentiated cells, in which the JNK phosphorylation increased about 160% by 6 h and that of p38 increased linearly to at least 18-fold throughout the cell death process. The increases in p38 and JNK phosphorylation were implicated in the death of the cells, since the p38 inhibitor PD169316 and the JNK inhibitor SP600125 were protective. These results demonstrate that the state of differentiation of PC12 cells, a model for the differentiation of sympathetic neurons, determines their vulnerability to cell death by modifying the state of phosphorylation and the regulation of specific kinases implicated in signal transduction pathways that are responsible for the survival or the death of these cells

Corrigendum to ‘SJS/TEN 2019: From science to translation’ [J. Dermatol. Sci. 98/1 (2020) 2–12]: From science to translation’ (Journal of Dermatological Science (2020) 98(1) (2–12), (S0923181120300645), (10.1016/j.jdermsci.2020.02.003)

The authors regret not all contributing authors correctly acknowledged funding. Jonathan Peter's IMARI-Africa project (AFRISCAR) is part of the EDCTP2 programme supported by the European Union (grant number TMA2017SF-1981). The authors would like to apologise for any inconvenience caused