Scaled experiments, w h o s e design was based on recently published low values for the viscosity of natural rocksalt, suggest that under typically low geological extension rates, a salt layer 500 m thick or thicker decouples the brittle overburden from the faulted basement. Because of its low viscosity, salt cannot transmit the large differential stresses necessary for basement faults to propagate upward as faults or abrupt forced folds into the brittle overburden, unless the salt layer is thin or has b e e n depleted. Thick salt diffuses localized deformation in the basement by flowing away from rising basement blocks, and toward sinking basement blocks. Basement extension is not transmitted to the overburden vertically but is laterally transmitted from the margins as the salt basin widens. Rather than being controlled by basement faults, the distribution of faults and diapirs in the overburden is controlled by lateral changes in overburden stratigraphy or thickness, preexisting faults, and faults that propagate laterally into the salt basin.

Osteoarthritis (OA) is characterized by progressive destruction of articular cartilage, resulting in significant disability. Chondrocytes present in various types of cartilage and are responsible for the growth and maintenance of the tissue. Over-proliferation of human chondrocytes may contributes to OA pathological process. Previously, we revealed that miR-127-5p could inhibit the proliferation of human chondrocytes through osteopontin (OPN). In the present study, we used online tools to figure out several candidates lncRNAs which were potentially correlated with miR-127-5p. Through assessing the expression levels of the candidates lncRNAs, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was chosen as a further research subject. MALAT1 knockdown significantly repressed human OA chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt in OA chondrocytes. As verified by luciferase assays, MALAT1 directly bound to miR-127-5p to inhibit miR-127-5p expression. Then we achieved miR-127-5p inhibition through miR-127-5p inhibitor transfection; the miR-127-5p inhibition could promote chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt; in addition, the MALAT1 knockdown partially reversed the promotive effect of miR-127-5p inhibition on chondrocyte proliferation, OPN and PI3K/Akt signaling-related protein levels. Taken together, MALAT1 could directly bind to miR-127-5p to inhibit its expression, so as to rescue OPN expression and promote chondrocyte proliferation through PI3K/Akt pathway. Targeting MALAT1 so as to rescue miR-127-5p expression in OA might help to inhibit chondrocyte proliferation through miR-127-5p-mediated OPN regulation and downstream PI3K/Akt pathway.

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This review study indicates that JNK pathway plays an important role in development and progression of OA, and targeting the JNK pathway might be a potential approach for the treatment of OA in future.