Periostin, an extracellular matrix protein, is widely expressed in a variety of tissues and cells. It has many biological functions and is related to many diseases: for example, it promotes cell proliferation and differentiation in osteoblasts, which are closely related to osteoporosis, and mediates cell senescence and apoptosis in chondrocytes, which are involved in osteoarthritis. Furthermore, it also plays an important role in mediating inflammation and reconstruction during bronchial asthma, as well as in promoting bone development, reconstruction, repair, and strength. Therefore, periostin has been explored as a potential biomarker for various diseases. Recently, periostin has also been found to be expressed in intervertebral disc cells as a component of the intervertebral extracellular matrix, and to play a crucial role in the maintenance and degeneration of intervertebral discs. This article reviews the biological role of periostin in bone marrow-derived mesenchymal stem cells, osteoblasts, osteoclasts, chondrocytes, and annulus fibrosus and nucleus pulposus cells, which are closely related to spinal degenerative diseases. The study of its pathophysiological effects is of great significance for the diagnosis and treatment of spinal degeneration, although additional studies are needed.
Intervertebral disc (IVD) degeneration (IVDD) is closely linked to degenerative spinal disease, resulting in disability, poor quality of life, and financial burden. Apoptosis of nucleus pulposus (NP) cells (NPCs) is a key pathological basis of IVDD. Periostin (POSTN), an extracellular matrix protein, is expressed in many tissues, whereas its abnormal expression is associated with IVDD. The conventional Wnt/β‐catenin pathway is also involved in IVDD and contributes to NPCs apoptosis. However, research on the mechanisms of POSTN in IVDD is lacking. This study investigated the relationship between POSTN and β‐catenin expression in degenerated IVDs. We detected the expression of POSTN, β‐catenin, and cleaved‐caspase‐3 (C‐caspase3) in degenerated and non‐degenerated IVD tissues of different grades (n = 8) using RT‐qPCR, immunohistochemical staining, and western blotting analysis. Next, we explored the effects of recombinant periostin (rPOSTN) and isoquercitrin (Iso), an inhibitor of the Wnt/β‐catenin pathway, on NPCs apoptosis. Finally, we inhibited the expression of POSTN in degenerated NPCs in vivo and investigated the anti‐apoptotic effect. The expression of β‐catenin, POSTN, and C‐caspase3 in severe degenerative IVDs was significantly higher than that in mild degenerative IVDs. These findings were confirmed in rat and cell‐based degenerative models. When treated with rPOSTN, the Wnt/β‐catenin pathway activity and cell apoptosis were time‐ and dose‐dependent. However, rPOSTN‐induced NPCs apoptosis decreased after iso‐induced inhibition of the Wnt/β‐catenin pathway. POSTN inhibition reduced apoptosis but was restored by rPOSTN re‐addition. Lastly, POSTN inhibition ameliorated puncture‐induced IVDD in vivo. Overall, our study demonstrated that POSTN promotes NPCs apoptosis and aggravates degeneration by activating the Wnt/β‐catenin pathway.
As a newly discovered mechanosensitive ion channel protein, the piezo1 protein participates in the transmission of mechanical signals on the cell membrane and plays a vital role in mammalian biomechanics. Piezo1 has attracted widespread attention since it was discovered in 2010. In recent years, studies on piezo1 have gradually increased and deepened. In addition to the discovery that piezo1 is expressed in the respiratory, cardiovascular, gastrointestinal, and urinary systems, it is also stably expressed in cells such as mesenchymal stem cells (MSCs), osteoblasts, osteoclasts, chondrocytes, and nucleus pulposus cells that constitute vertebral bodies and intervertebral discs. They can all receive external mechanical stimulation through the piezo1 protein channel to affect cell proliferation, differentiation, migration, and apoptosis to promote the occurrence and development of lumbar degenerative diseases. Through reviewing the relevant literature of piezo1 in the abovementioned cells, this paper discusses the effect of piezo1 protein expression under mechanical stress stimuli on spinal degenerative disease, providing the molecular basis for the pathological mechanism of spinal degenerative disease and also a new basis, ideas, and methods for the prevention and treatment of this degenerative disease.
Here we use a pseudoallyl ligand, N,N′-chelating amidinate (Am), together with pentamethylcyclopentadienyl
(Cp*) to give two dysprosium(III) single-molecule magnets (SMMs):
[{(AmiPr)DyCp*(μ-Cl)}2] and [AmdippDyCp*(Cl)(μ-Cl)Li(THF)3] with distinct energy barriers
(U
eff) of 97 and 472 K, respectively.
The latter U
eff value is similar to the
homoleptic Cp*-based Dy-SMM.
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