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Synthesis of cationic polymers possessing significant therapeutic potential is of tremendous research interest. Here, we report a facile synthesis of poly(e-caprolactone) (PCL) based cationic polymers with controlled topological structures and tunable charge densities via postpolymerization modification using thio-bromo “click” chemistry. Three types of polymeric precursors were prepared by ring-opening polymerization (ROP) or combination of ROP and azide–alkyne click reaction, including linear homopolymer poly(α-bromo-e-caprolactone) (P(CL-Br)), block copolymer PCL-b-P(CL-Br), and bottlebrush polymer PCL-g-(PCL-b-P(CL-Br)), and then the P(CL-Br) blocks or segments were modified using the thio-bromo click reaction with a thiol bearing a tertiary amino group, yielding the corresponding cationic polymers, respectively. Size exclusion chromatography (SEC) and 1H NMR characterization demonstrated successful synthesis of the cationic polymers with controlled molecular weights and topological structures that may have great potential for biomedical applications.

The stability of surface-tethered polyelectrolyte brushes has been investigated during the past few years. We have previously reported on the degrafting of poly(acrylic acid) (PAA) polymer brushes from flat silicon substrates. Here, we present a detailed study on the effects of NaCl concentration and the grafting density and molecular weight on the stability of PAA brushes during incubation in 0.1 M ethanolamine buffer (pH 9.0) solutions. Without NaCl in the buffer solution, the PAA brushes remain intact. Adding NaCl facilitates etching of the substrate due to accelerating dissolution of the top silica layer and promoting degrafting of the PAA chains. The PAA grafting density and molecular weight play an important role in the substrate etching by affecting the penetration barrier and local concentration of the etchants. We also tested the stability of self-assembled monolayers (SAMs) made of hydrophobic alkyltrichlorosilanes anchored on silicon substrates. The results demonstrated that the SAMs were too thin to protect the substrates from etching, in contrast to thick poly(methyl methacrylate) brushes. Our findings suggest that both polymer brushes (especially polyelectrolyte brushes) and SAMs anchored to silicon substrates may undergo erosion/etching on the substrates in basic environments, which compromises their stability and therefore jeopardizes their applications in coating, biosensing, and so forth.

Molecular bottlebrushes featuring brush-on-brush (BoB) architecture were prepared by combining azide-alkyne click chemistry, ring-opening polymerization (ROP), and atom transfer radical polymerization (ATRP). Primary side chains of diblock copolymers with a poly(ε-caprolactone) (PCL) block and a poly(α-bromo-ε-caprolactone) (P(CL-Br)) block were synthesized by ROP and then grafted onto PCL backbone by the click reaction. Then the secondary side chains of poly(oligo(ethylene glycol) acrylate) (POEGA) were grafted from the P(CL-Br) block by ATRP, yielding an amphiphilic core/shell structure. Imaging of individual macromolecules by atomic force microscopy (AFM) demonstrated dramatically thickened wormlike formation with distinct hairy side chains. Interestingly, for the BoB molecular bottlebrushes with enough long primary and secondary side chains, sufficient tension can be generated along the backbone and thus lead to its cleavage.

In vivo, cardiomyocytes comprise a heterogeneous population of contractile cells defined by unique electrophysiologies, molecular markers and morphologies. The mechanisms directing myocardial cells to specific sub-lineages remain poorly understood. Here we report that overexpression of TGFβ-Activated Kinase (TAK1/Map3k7) in mouse embryonic stem (ES) cells faithfully directs myocardial differentiation of embryoid body (EB)-derived cardiac cells toward the sinoatrial node (SAN) lineage. Most cardiac cells in Map3k7-overexpressing EBs adopt markers, cellular morphologies, and electrophysiological behaviors characteristic of the SAN. These data, in addition to the fact that Map3k7 is upregulated in the sinus venous-the source of cells for the SAN-suggest that Map3k7 may be an endogenous regulator of the SAN fate.