Cell and Tissue Research最新文献

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterised by several factors, such as impaired glutamate neurotransmission affecting crucial functions. Neural stem cells (NSCs) are present in the adult brains of all mammalian species and contribute to the continuous generation of neural cells throughout life. The disruption of glutamate levels during the development of AD could impact NSCs' functionality, influencing their response to the microenvironment. In this work, we isolated adult neural stem cells from both triple transgenic (3xTg)-AD mice and age-matched wild type (WT) mice in order to gather information on any differences between them, particularly concerning the potential mechanisms involved in the internalisation of glutamate and its utilisation for energy production. The 3xTg model offers the ability to recapitulate human pathology with both plaque and tangle hallmarks that are involved in the process of glutamate release. In vitro culture 3xTg NSCs showed a slight morphological difference compared to WT cells and a massive reduction of proliferation and viability. Furthermore, 3xTg NSCs displayed an increase in the expression of glutamate transporters and glutamine synthetase, while glutamate dehydrogenase did not show any reduction, which is typical in AD brains. Data obtained from this basic research study suggest a possible involvement of glutamate in the cellular energy balance, indicating an attempted response of NSCs to the cytotoxic microenvironment in the early stage of AD pathology. This finding is of great interest, as it corroborates the hypothesis that targeting the glutamatergic system could be an extremely promising strategy for new therapeutics in AD.

Microtubules are the principal cytoskeletal component in cells, integral to various morphogenetic processes in Metazoa, including cell migration, adhesion, and polarity. Their dynamics and functions are modulated by tubulin post-translational modifications (PTMs). While studies on model species have provided insights into microtubule functions, understanding their evolutionary aspects necessitates exploring non-model organisms. Sponges (phylum Porifera) are an early-branching metazoan group with outstanding regenerative capacities. This research presents the first comprehensive analysis of microtubule organization and tubulin PTMs in calcareous sponges. The intact sponge cells show various but typical types of microtubule organization, while detected tubulin PTMs are associated with certain cell types, indicating specific functions in particular cellular contexts. During regeneration, relying on the coordinated movement of epithelial-like cell sheets, microtubule networks in exopinacocytes and choanocytes undergo significant reorganization. These rearranged microtubules potentially stabilize cellular migration direction and facilitate cargo transport, essential for cell contact and polarity establishment. This study enhances our understanding of microtubule functionality and regulation in early-diverging metazoans, contributing to the broader evolutionary context of cytoskeletal dynamics.

Hydroxyapatite nanoparticle (HANPs) utilization has recently been notable in bone tissue engineering. This surge owes itself to the biocompatibility of HANPs and their striking resemblance to the minerals found in natural bone. Furthermore, dental pulp-derived stem cells (DPSCs) have garnered attention due to their remarkable differentiation potential into multilineages, thus positioning them as a pivotal cell reservoir for regenerative medicine. This study aims to investigate the impact of HANPs on DPSCs cellular processes. The HANPs have been synthesized using the wet chemical precipitation method followed by freeze-drying and characterization using dynamic light scattering (DLS) and transmission electron microscopy (TEM). The size of HANPs was reported to be in the range of 55-67 nm. Our dataset divulges that DPSCs can endure concentrations of HANPs up to ≤ 0.81 mg/mL without incurring any conspicuous alterations in their morphology or the pace of proliferation. Furthermore, the self-renewal potency of HANPs was upheld at concentrations ≤ 0.20 mg/mL. Flow cytometric analysis affirms a significant divergence in cell distribution across all cell cycle phases in DPSCs treated with 0.81 mg/mL HANPs. Intriguingly, no variance surfaced in the migratory capacity of DPSCs exposed to HANPs of ≤ 0.40 mg/mL. For osteogenic differentiation, HANPs at concentrations of ≤ 0.40 mg/mL demonstrated the aptitude to incite osteogenic differentiation within DPSCs, facilitating the formation of calcium deposits. In conclusion, combining HANPs and DPSCs shows promise for restoring damaged hard tissues, like bone and teeth, and enhancing regenerative therapies.

The mucosal epithelium and the mucosa-associated lymphoid tissues (MALTs) protect the mucosa, such as eye and nose, from constant exposure to foreign antigens. As autoimmune disorders can target both epithelium and MALTs, we morphologically investigated the head of MRL/MpJ-Fas^lpr/lpr, an autoimmune disease-prone mouse, to discuss the pathological crosstalk among autoimmune disorders, mucosal epithelium, and MALTs. Compared to healthy control MRL/MpJ mice, MRL/MpJ-Fas^lpr/lpr mice had more lymphoid tissues that were diffusely localized beneath the mucosa epithelium in their lacrimal tracts and nasal cavity. Particularly, lacrimal duct- and nasopharynx-associated lymphoid tissues (LDALT, NALT) were identified as the major MALTs in the mouse head. In the nasal mucosa, MRL/MpJ-Fas^lpr/lpr mice exhibited larger NALT, more frequent non-ciliated epithelial cells, and more goblet cells than in MRL/MpJ mice. NALT in MRL/MpJ-Fas^lpr/lpr mice contained more proliferating cells than in MRL/MpJ mice. Moreover, LDALT in some MRL/MpJ-Fas^lpr/lpr mice developed by being directly connected to the bone marrow surrounding the nasolacrimal duct. These data suggested systemic autoimmune disorders could alter the mucosal immunity of the head by affecting both mucosal epithelium and MALTs. These findings are crucial for understanding the pathology of the head mucosal immunity.

Obesity has been associated with lower muscle strength-to-body mass ratio. Here, we evaluated the effects of diet-induced obesity on the mechano-structural properties of isolated muscles and tendons. Thirty 10-week-old male C57BL/6 J mice were randomly assigned to either an obesogenic high-fat diet group (OB) for 24 weeks or a control group (CN) maintained on a standard chow diet. Soleus muscle (SOL) and Achilles tendon (AT) specimens were isolated and subjected either to failure testing, 300 cycles of passive stretch-destretch, or isometric twitch contractions. Morpho-structural and protein expression analyses were conducted to assess collagen and adipose tissue accumulation, concentrations of cross-linking factors, and any alterations in the POSTN-TGFβ1-Akt signaling pathway. OB SOL and AT tissues were more fragile than those from CN (p < 0.05). A piecewise linear regression model revealed a tendency for OB tissues to exhibit steeper mechanical property changes within the first 20 cycles compared to CN, followed by a similar plateau phase in both groups. OB SOL-AT complexes showed a slower twitch-contraction-relaxation pattern than CN (p < 0.05). OB tendons and muscles were larger than those of the CN, with muscles featuring bigger fibers, and higher collagen area fraction (p < 0.05). Elevated TGFβ1 and POSTN concentrations were observed in OB tissues (p < 0.05), alongside increased P-Akt and P-4EBP1 expression (p < 0.05). These findings highlight the detrimental effects of obesity on the structural integrity of muscle and tendon tissues and suggest a significant role of POSTN-TGFβ1-Akt signaling in obesity-associated musculotendinous remodeling.

Constipation and other digestive disorders are common in older adults. The autonomic nervous system plays a critical role in regulating digestive motility in the intestinal tract. However, studies on age-related changes in autonomic function and receptor expression in the intestinal tract are limited. In this study, we examined the expression of neurotransmitter receptors in the autonomic nervous system and the effects of acetylcholine and β-agonists on intestinal contraction and relaxation in the jejunum of aged rats. Jejunal sections collected from male and female Wistar/ST rats aged 4, 11, and 18 months were analyzed. Immunohistochemical staining and enzyme-linked immunosorbent assay were used to measure the expression of muscarinic acetylcholine receptors (CHRM2 and CHRM3) and β-adrenergic receptors (β2-ADR and β3-ADR). The effects of acetylcholine, isoproterenol, and mirabegron were assessed in the isolated jejunum for each age group. There was no significant difference in CHRM2 receptor expression among the age groups; however, CHRM3 receptor expression decreased with age. Additionally, the sensitivity to acetylcholine-induced contractile responses decreased with age. Although β2-ADR receptor expression did not differ among the age groups, β3-ADR receptor expression increased with age. Despite this, the relaxation response to isoproterenol and mirabegron decreased with age. Our study revealed an age-related decrease in CHRM3 expression and the contractile response to acetylcholine in the small intestine of rats. Although β-ADR expression, particularly β3-ADR, increased with age, the relaxation response to β-adrenergic agonists gradually decreased.

The Kupffer cell was first discovered by Karl Wilhelm von Kupffer in 1876, labeling them as "Sternzellen." Since their discovery as the primary macrophages of the liver, researchers have gradually gained an in-depth understanding of the identity, functions, and influential role of Kupffer cells, particularly in infection. It is becoming clear that Kupffer cells perform important tissue-specific functions in homeostasis and disease. Stationary in the sinusoids of the liver, Kupffer cells have a high phagocytic capacity and are adept in clearing the bloodstream of foreign material, toxins, and pathogens. Thus, they are indispensable to host defense and prevent the dissemination of bacteria during infections. To highlight the importance of this cell, this review will explore the history of the Kupffer cell in the context of infection beginning with its discovery to the present day.

Carl C. Speidel (1919) and Ernst Scharrer (1928) were privileged witnesses of the encounter between neurons and hormones, a biological phenomenon that had been occurring in nature during millions of years of evolution, as Berta Scharrer started to unfold since 1935 on. The story of neurosecretion is intimately associated to that of the hypothalamus, such a "marvellous region", as Wolfgang Bargmann (1975) called it. This story started more than two millennia ago. We have made an effort to trace the roots of the discoveries that gave rise to a medical discipline, neuroendocrinology. Our trip to the roots covers a period from the fourth century BC, when an extraordinary Medical School was founded in Alexandria, and extends into the late 1970s of the twentieth century, when neuroendocrine research had started to grow exponentially. An effort has been made to track back the origin of each piece of knowledge that was constructing, brick upon brick, the building of this new medical science, hoping that it would help neuroendocrinologists of the new era to find their own roots, to meet their ancestors. Tracking the roots of a particular phenomenon provides the opportunity to have an overview of the whole phenomenon, allowing comprehension rather than merely knowledge. An important purpose pursued throughout this article was to pay a tribute to all those who, in the early days, contributed to the brain-endocrine encounter. We have tried our best to bring back the achievements of most of them.