Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • Already in Okumura et al reported that

    2018-10-20

    Already in 2001 Okumura et al. reported that increased FAK phosphorylation on Ti surfaces during osteogenic differentiation is directly linked to re-arrangement of the LY 2157299 cytoskeleton (Okumura et al., 2001). In order to investigate potential differences in actin cytoskeleton architecture between ITSCs cultivated on nanoporous Ti substrate (30nm pores) and on flat Ti, we stained F-actin using Rhodamine-coupled phalloidin. In our approach we observed highly ordered, polarized cytoskeletal fibers in ITSCs on 30nm pores, which is consistent with re-arrangement of cytoskeleton during osteogenic differentiation (reviewed in (Chen and Jacobs, 2013)).
    Conclusions In sum, we were able to show that cultivation of human neural crest-derived ITSCs on a nanoporous titanium surface with an anisotropic arrangement of 30nm pores leads to osteogenic differentiation without the need of additional biochemical cues. This nanotopologically induced osteogenic differentiation is accompanied by up-regulation of Integrin subunits α2 and β1, Bmp2, Osterix and Osteocalcin. In addition, we demonstrated high activity of alkaline phosphatase, increased phosphorylation of FAK at Y397, re-arrangement of actin cytoskeleton and finally significantly elevated Ca deposition by differentiated cells (summarized in Fig. 6). In the future, this approach could be used to improve the integration of prostheses via populating with autologous, osteogenically pre-differentiated neural crest-derived cells. The following are the supplementary data related to this article.
    Acknowledgments The excellent technical help of Angela Krahlemann-Köhler is gratefully acknowledged. This study was supported by the University of Bielefeld and by a Grant of the German Ministry of Research and Education to BK (BMBF, Grant: 01GN1006A). The authors acknowledge the support for the Article Processing Charge by the Deutsche Forschungsgemeinschaft (DFG) and the Open Access Publication Funds of Bielefeld University Library. We thank Holger Sudhoff for providing human inferior turbinates.
    Introduction In all eukaryotes, DNA is tightly associated with histone proteins in order to form chromatin, of which the fundamental subunit is the nucleosome (Luger et al., 1997). Each nucleosome consists of four different core histone types (H2A, H2B, H3 and H4), which have been very well evolutionarily conserved. Chromatin structure is essential for compaction of genomic DNA but also represents a physical barrier to control DNA accessibility and gene expression. In embryonic stem cells (ESC) the delicate balance of self-renewal and differentiation into specific lineages is determined by many lineage-restricted promoters that are associated with highly combinatorial posttranslational histone modification (PTM) patterns which may determine their selective priming of gene expression during lineage commitment. Together with DNA methylation, ATP-dependent chromatin remodeling, RNA interference, non-coding RNA and incorporation of histone variants, these properties form the “epigenetic signature” (Tollervey and Lunyak, 2012). Not only ESC differentiation but also other biological contexts are characterized by a continuous interplay of installation and removal of histone PTMs. To accomplish the latter, several mechanisms can be at play. Apart from enzymatic elimination of modifications (Kouzarides, 2007; Tollervey and Lunyak, 2012) and histone exchange (Bernstein and Hake, 2006; Skene and Henikoff, 2013; Tollervey and Lunyak, 2012), also regulated proteolytic histone cleavage has been suggested to play such role (Duncan and Allis, 2011; Duncan et al., 2008). Duncan et al. showed that H3 is proteolytically cleaved at its N-terminus during early differentiation of mouse ESC (mESC) and they provide evidence for the regulatory capacity of covalent modifications herein (Duncan et al., 2008). Cathepsin L was found to cleave histone H3, with alanine 21 being the primary site of cleavage (Adams-Cioaba et al., 2011; Duncan et al., 2008). This truncated H3 form is detected during the first days of both monolayer differentiation (with and without retinoic acid induction) and embryonic body (EB) formation. Similar clipping events of H3 associated with other cellular processes including viral infection (Falk et al., 1990; Tesar and Marquardt, 1990), aging (Gonzalo, 2010; Mahendra and Kanungo, 2000) and sporulation (Santos-Rosa et al., 2009) have also been reported. Additionally, H3 protease activity was also found in chicken liver and Tetrahymena micronuclei (Allis and Wiggins, 1984; Allis et al., 1980; Mandal et al., 2012, 2013). Although the molecular consequences of any histone clipping event are yet to be defined, these data seem to suggest an evolutionary conserved process.