scispace - formally typeset
Search or ask a question

What role do stromal cells play in regulating the bone marrow microenvironment? 


Best insight from top research papers

Stromal cells in the bone marrow microenvironment are pivotal in regulating hematopoiesis and influencing disease development. These cells, including mesenchymal stromal cells (MSCs), communicate with hematopoietic stem cells through cytokines, growth factors, and extracellular vesicles, impacting normal and malignant hematopoiesis. Genetic and functional alterations in stromal cells can contribute to leukemogenesis, creating a niche supportive of myeloid neoplasms. Single-cell technologies aid in dissecting the interactions between stromal cells and malignant hematopoiesis, offering insights for potential therapeutic strategies. Additionally, the extracellular matrix (ECM) produced by stromal cells plays a crucial role in coordinating cellular phenotypes within the niche, influencing cell maintenance and phenotype. Overall, stromal cells are essential regulators of the bone marrow microenvironment, impacting hematopoiesis and disease progression.

Answers from top 5 papers

More filters
Papers (5)Insight
Open accessBook ChapterDOI
08 Mar 2023
Stromal cells regulate the bone marrow microenvironment by communicating with neighboring cells through cytokines, growth factors, and extracellular vesicles, crucial for haematopoiesis and potentially impacting cancer development and metastasis.
Stromal cells, particularly mesenchymal stromal cells and osteoblastic derivatives, influence normal hematopoiesis and contribute to myeloid malignancies by creating a supportive niche for leukemic cells in the bone marrow.
Stromal cells in the bone marrow regulate hematopoiesis through distinct mechanisms, including niche organization, cell differentiation hierarchy, and cell-cell communication, influencing the bone marrow microenvironment.
Stromal cells, particularly mesenchymal stromal cells and osteoblastic derivatives, influence normal hematopoiesis and contribute to myeloid malignancies by supporting leukemogenesis and creating a niche for neoplastic cells.
Stromal cells in the bone marrow regulate cell phenotype through secreted extracellular matrix proteins, influencing niche maintenance and cell behavior, highlighting their crucial role in the bone marrow microenvironment.

Related Questions

How tams affect stromal cells in hcc?5 answersTumour-associated macrophages (TAMs) play a crucial role in the tumour microenvironment of hepatocellular carcinoma (HCC). TAMs can interact with stromal cells, such as liver myofibroblasts (aLMFs), affecting HCC progression. In the context of HCC, TAMs have been shown to promote the development of epithelial-mesenchymal transition (EMT), proliferation, and migration of HCC cells. Additionally, TAMs in HCC have been associated with alternative activation and the release of pro-metastatic mediators, while tumor-associated neutrophils (TANs) have been linked to angiogenesis and tumor detachment. Furthermore, the expression of Tim-3 in TAMs has been found to significantly impact the activation and function of TAMs, influencing HCC cell growth both in vitro and in vivo. These interactions between TAMs and stromal cells highlight the complex dynamics within the HCC microenvironment.
How immuno property of MSC influence tissue regeneration?5 answersMesenchymal stem cells (MSCs) possess immunomodulatory properties that influence tissue regeneration. The immunomodulatory effects of MSCs are mediated through various mechanisms such as cell-cell contact, cytokine secretion, and extracellular vesicles (EVs). MSCs interact with immune cells and modulate their phenotype and function, leading to tissue repair and regeneration. The immunomodulatory properties of MSCs include the suppression of pro-inflammatory markers and the elevation of reparatory markers in immune cells. MSCs also produce pro-angiogenic factors and promote neo-vascularization, contributing to enhanced tissue repair and regeneration. The EVs secreted by MSCs play a role in their immunomodulatory function, as evidenced by changes in the miRNA composition of EVs in response to inflammatory signals. Overall, the immunomodulatory properties of MSCs play a crucial role in tissue regeneration by regulating the immune response and promoting tissue repair and angiogenesis.
Which pathway associated with bone marrow mesenchymal stromal cell may be responsible for severity of multiple myeloma?4 answersThe severity of multiple myeloma may be associated with the TNF signaling via NF-kB and Inflammatory response pathways in bone marrow mesenchymal stromal cells (BMSCs). These pathways are activated in the presence of multiple myeloma cells and contribute to the development of drug resistance and the pro-tumorigenic microenvironment in multiple myeloma. The upregulation of heme oxygenase-1 (HO-1) in BMSCs also plays a role in promoting the survival and growth of multiple myeloma cells, potentially through the CXCL12/CXCR4 signaling pathway. Additionally, the expression of programmed cell death ligand 1 (PD-L1) on BMSCs may induce apoptosis of CD8+ T cells and promote immune escape in multiple myeloma. The expression of steroid receptor coactivator 3 (SRC3) in BMSCs can enhance the proliferation, survival, and adhesion abilities of multiple myeloma cells through various signaling pathways. These findings suggest that targeting these pathways in BMSCs may be a potential strategy for the treatment of multiple myeloma.
Bone marrow microenvironment and its significance in Multiple myeloma?5 answersThe bone marrow microenvironment plays a significant role in the pathogenesis of multiple myeloma (MM) and is actively involved in promoting tumor growth and progression. Multiple myeloma cells interact with various cell populations within the bone marrow, including immune and non-immune cells, as well as the extracellular matrix. These interactions contribute to the survival, proliferation, and chemotherapeutic resistance of MM cells. The bone marrow microenvironment also supports the homing and dissemination of MM cells to the bone marrow niche. Several signaling pathways and molecules, such as Roundabout 1 (ROBO1) and cyclophilin A (CyPA), have been identified as important players in MM-bone marrow cross-talk. Targeting these pathways and molecules may provide new therapeutic strategies for MM treatment.
What is the impact of High fat diet on bone marrow MSC?5 answersHigh-fat diet (HFD) has been shown to have an impact on bone marrow mesenchymal stem cells (MSCs). HFD was found to decrease the population of lin-/CD117+ cells in the bone marrow (BM) of aging mice, which was associated with increased reactive oxygen species (ROS) production. In a study on mice, bone-specific PPARγ conditional knockout (cKO) prevented HFD-induced bone deterioration, indicating the role of PPARγ in regulating bone mass. HFD was also found to increase BM adiposity and decrease trabecular bone mass, leading to bone fragility. In rats, HFD was shown to induce alterations in MSCs, including increased production of pro-inflammatory cytokines and reduced expression of PPAR-γ, which could affect hematopoiesis. Furthermore, HFD-induced elevation of serum CXCL2 levels was found to impair BMSC functions, including adipogenesis, migration, and senescence. These findings suggest that HFD can negatively impact bone marrow MSCs, leading to changes in bone mass and adiposity, as well as alterations in hematopoiesis and MSC functions.
How does the M1 macrophage affects the MSCs?5 answersM1 macrophages have been shown to affect mesenchymal stem cells (MSCs) in several ways. In the myocardial infarction microenvironment, M1-type macrophage-derived exosomes induce apoptosis in MSCs by delivering miR-222 to them. M1 macrophages also promote the osteogenic differentiation of bone marrow MSCs (BMMSCs) better than M0 macrophages, and exosomes derived from M1 macrophages enhance the osteogenic capacity of BMMSCs by activating Akt and increasing RUNX2 levels. However, in the hypoxic environment typically observed in chronic wounds, hypoxia inhibits MSC-induced M1 to M2 macrophage transition, suggesting that hypoxic environments may impede the therapeutic effects of MSCs. Additionally, co-culture of MSCs with M2 macrophages, but not with M1 or M0 macrophages, results in increased MSC mineralization, indicating that M2 macrophages promote the osteogenic differentiation of MSCs. Overall, M1 macrophages can affect MSCs by inducing apoptosis, promoting osteogenic differentiation, and influencing macrophage polarization.

See what other people are reading

What is the mechanism of LINC01021-mediated cell inhibition of cell senescence?
5 answers
LINC01021 mediates cell inhibition of senescence by regulating the p53-p21 pathway. It interacts with BMI1 to repress MCP-1 transcription, activating the p53-p21 pathway and inhibiting senescence in human mesenchymal stromal and acute myeloid leukemia cells. Additionally, LINC01021 regulates KISS1 through CDK2, promoting CDX2 phosphorylation and nuclear export, ultimately promoting malignant cell migration and angiogenesis in gastric cancer. Conversely, Linc-ASEN prevents cellular senescence by reducing p21 production transcriptionally and posttranscriptionally, forming a complex with UPF1 to suppress p21 transcription and enhance p21 mRNA decay. These findings highlight the intricate mechanisms through which LINC01021 and Linc-ASEN modulate senescence pathways, offering potential therapeutic targets for diseases like cancer.
What is the elastic modulus of agarose gel with varying concentration?
5 answers
The elastic modulus of agarose gel varies with concentration. Studies have shown that higher agarose concentrations result in higher storage moduli. For instance, the storage modulus ranged from approximately 30 to 2300 kPa depending on the agarose concentration, with values increasing as the concentration increased. Additionally, the addition of agarose to composite hydrogels increased stiffness and relaxation time constants, indicating a direct correlation between agarose concentration and viscoelastic properties. Furthermore, the viscoelastic shear moduli of low concentrations of agarose gel were found to increase with frequency, showcasing the dynamic nature of the material's mechanical properties. Therefore, the elastic modulus of agarose gel is influenced by its concentration, with higher concentrations generally leading to higher storage moduli.
Are IL-6 and MPO interconnected in the development and progression of prostate cancer?
5 answers
IL-6 and MPO (Myeloperoxidase) are interconnected in the development and progression of prostate cancer. IL-6, a pleiotropic cytokine, is predominantly expressed in the stromal compartment of the prostate, including endothelial cells and macrophages, suggesting a paracrine role in disease progression. On the other hand, MPO, an enzyme primarily found in neutrophils, plays a crucial role in the inflammatory processes associated with prostate tumors. The inflammatory microenvironment in prostate cancer, characterized by the overexpression of inflammatory processes and the accumulation of immunocompetent cells, contributes to tumor development and progression. Additionally, studies indicate that cytokines like IL-6 and IL-8 are potential biomarkers for prostate cancer pathogenesis, with elevated levels correlating with disease progression. Therefore, the interplay between IL-6 and MPO within the inflammatory context of prostate cancer underscores their interconnected role in disease advancement.
How does the speed of surgical intervention for a ruptured calcaneal tendon affect functional recovery?
5 answers
The speed of surgical intervention for a ruptured calcaneal tendon significantly impacts functional recovery. Studies have shown that early accelerated functional rehabilitation combined with percutaneous minimally invasive suture treatment for acute closed Achilles tendon rupture (ACATR) can accelerate Achilles tendon function recovery without increasing complications. Surgical repair after acute Achilles tendon rupture, especially through minimal invasive surgery, leads to lower re-rupture rates than non-surgical treatment. Additionally, the use of a common calcaneal tendon cadaver allograft with subsequent application of platelet-rich plasma for chronic ruptures has shown complete functional recovery after long-term follow-up. Immediate full weightbearing and ankle motion exercise post-repair of acute Achilles tendon rupture have also been associated with low re-rupture rates and satisfactory functional outcomes. These findings collectively emphasize the importance of prompt surgical intervention for optimal functional recovery post-calcaneal tendon rupture.
What activates myfibroblasten?
5 answers
Myofibroblasts are activated by various stimuli, leading to their secretory and contractile phenotype. Activation traditionally involved the de novo expression of alpha-smooth muscle actin stress fibers, previously viewed as a binary process. Recent studies have shifted towards considering myofibroblast activation as a continuous spectrum, necessitating a method to quantify this activation level. Mechanisms of myofibroblast activation include responses to changes in the cytokine milieu and extracellular matrix composition, leading to dynamic phenotypic alterations. Additionally, compounds like cyclolanostane and rophenol have been identified as fibroblast activators, promoting the production of collagen and other extracellular matrix components. These findings collectively highlight the multifaceted nature of myofibroblast activation and the diverse pathways involved in their stimulation.
What are dendritic cells?
4 answers
Dendritic cells (DCs) are professional antigen-presenting cells derived from hematopoietic stem cells, crucial for immune responses. They play a central role in bridging innate and adaptive immunity by capturing antigens, presenting them to T lymphocytes, and determining immune activation or anergy. DCs are essential in priming the adaptive immune response and are targets for immune-based therapeutic approaches, especially in cancer treatment. In the context of HIV infection, DCs are among the first cells encountered by the virus and have shown promise in triggering immune responses against the virus, making them potential candidates for vaccine development. Understanding the complexity of DC subsets, functions, and responses is crucial for harnessing their full potential in immunotherapy and vaccine strategies.
Why is the philadelphia chromosome only found in blood cells?
7 answers
The Philadelphia chromosome (Ph) is a specific genetic abnormality characterized by a reciprocal translocation between chromosome 9 and chromosome 22, leading to the formation of a truncated chromosome 22. This chromosomal aberration is the hallmark of chronic myeloid leukemia (CML) and is also found in various other leukemias, including acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic neutrophilic leukemia (CNL), and mixed phenotype acute leukemia (MPAL). The Ph chromosome results from aberrant ligation between two DNA double-strand breaks at the BCR gene on chromosome 9q34 and the ABL1 gene on chromosome 22q11, which are crucial initiation events for oncogenesis in Ph-positive leukemia. The presence of the Ph chromosome in blood cells is attributed to its origination in a pluripotential stem cell, affecting myeloid, megakaryocytic, and erythroid lineages. This suggests that the translocation disrupts genomic stability and impairs physiological signaling pathways in these cells, leading to their malignant transformation. The specific detection of the Ph chromosome in blood cells, rather than other cell types, is due to the nature of the affected stem cells that give rise to the blood cell lineages. Techniques such as karyotyping, Fluorescence in Situ Hybridization (FISH), and PCR are employed to diagnose the presence of the Ph chromosome, highlighting its detection primarily in blood cells. Moreover, the Ph chromosome's association with blood cell malignancies is further evidenced by its role in the pathogenesis of diseases like CML, where it is found in more than 90% of patients, and in ALL, where it significantly affects prognosis and treatment outcomes. The development of specific detection frameworks using image processing and deep learning techniques aims to improve the diagnosis of the Philadelphia chromosome, emphasizing its significance in blood cell disorders. Additionally, the Ph chromosome's impact on the clinical presentation and cellular biology of different phenotypes of Ph-positive leukemia underlines its critical role in the malignant transformation of blood cells. In summary, the Philadelphia chromosome is found exclusively in blood cells due to its origination from a mutation in pluripotential stem cells that differentiate into various blood cell lineages, leading to the development of specific leukemias where this genetic abnormality plays a pivotal role in disease progression and treatment response.
What are the potential therapeutic strategies for preventing or treating eryptosis in sickle cell disease?
5 answers
Potential therapeutic strategies for preventing or treating eryptosis in sickle cell disease (SCD) include targeting oxidative stress, calcium activity, ceramide pathways, and fetal hemoglobin reactivation. Oxidative stress plays a crucial role in accelerating eryptosis in SCD patients, leading to increased calcium activity and phosphatidylserine externalization. Additionally, the ceramide pathway is implicated in triggering eryptosis in SCD. Furthermore, reactivating fetal hemoglobin through gene therapy has shown promise in reducing HbS levels and correcting the sickling phenotype in SCD patients. Developing multi-agent strategies based on SCD pathophysiology is crucial for enhancing the quality of life and survival of individuals with SCD. These combined approaches offer a comprehensive way to address the complex mechanisms underlying eryptosis in SCD.
What is the biggest advancement in tissue engeneering?
5 answers
The most significant advancement in tissue engineering lies in the utilization of cutting-edge technologies such as three-dimensional bioprinting, organ-on-a-chip systems, and induced pluripotent stem cell technologies. These innovations have revolutionized the field by enabling the creation of complex tissue constructs for regenerative medicine and disease modeling. Additionally, the development of biologically active scaffolds based on extracellular matrix analogues has played a crucial role in tissue and organ regeneration. Tissue engineering aims to restore or construct whole tissues using mesenchymal stem cells, signaling molecules, and scaffolds, reducing the need for extensive reconstructive surgery. The focus on functional product development anchored in disease state needs, along with collaborative research efforts, has shown significant translational potential in tissue engineering.
What is the significance of c-myc rearrangement in T cell ALL?
5 answers
C-MYC rearrangement in T-cell Acute Lymphoblastic Leukemia (T-ALL) holds significant clinical and prognostic implications. Studies have shown that C-MYC protein expression is prevalent in T-ALL cases, with a notable association with aggressive disease behavior and poor prognosis. While C-MYC gene abnormalities like gene rupture and copy number increase are not common in T-ALL, the expression of C-MYC protein itself is linked to adverse outcomes, indicating its potential as an independent prognostic factor. Furthermore, the presence of C-MYC protein and genetic abnormalities together in T-ALL cases is associated with even worse prognosis, highlighting the importance of assessing C-MYC status for risk stratification and treatment decisions in T-ALL patients.
Isocitrate dehydrogenase in TCA cycle
4 answers
Isocitrate dehydrogenase (IDH) plays a crucial role in the tricarboxylic acid (TCA) cycle. There are different isoforms of IDH, such as IDH2 and IDH3, each with specific functions. IDH2 is essential for promoting leukemia cell survival and proliferation in acute myeloid leukemia (AML) by facilitating lipid synthesis. On the other hand, IDH3 is vital for the production of α-ketoglutarate (α-KG) from isocitrate in the TCA cycle and is implicated in regulating metabolism in various tissues, including the testes where it influences spermiogenesis. Additionally, IDH3A, a subunit of the IDH3 heterotetramer, is upregulated in hepatocellular carcinoma (HCC) and contributes to HCC progression by promoting epithelial-mesenchymal transition (EMT) through the upregulation of metastasis associated 1 (MTA1).