ESC
iPSC — Cardiac

iPSC-Derived Cardiomyocytes

I generate iPSC-derived cardiomyocytes (iPSC-CMs) using Wnt-modulated GiWi differentiation followed by lactate-based metabolic enrichment. The resulting beating monolayers and 3D micro-tissues support disease modeling for inherited arrhythmias, hypertrophic and dilated cardiomyopathies, and routine cardiotoxicity profiling on MEA, calcium imaging, and impedance-based contractility platforms.

GiWi Protocol cTnT & Sarcomeres MEA / FPD Contractility Detailed Methods RNA-seq
01

Wnt-Modulated (GiWi) Cardiac Differentiation

Sequential Wnt activation (Day 0–2 with CHIR99021) followed by Wnt inhibition (Day 3–5 with IWP-2 or Wnt-C59) drives high-efficiency cardiomyogenesis through mesoderm. Spontaneous beating typically appears by Day 8–10. Lactate-medium selection from Day 10–14 enriches cardiomyocytes by exploiting their unique ability to oxidize lactate for ATP production.

Differentiation Timeline
iPSC → Mesoderm → Cardiac Progenitor → Cardiomyocyte → Mature CM
Day −2 to 0
iPSC Plating
OCT4 · NANOG
Plate at confluence on Matrigel in mTeSR1 + ROCK-i.

Single-cell dissociate; plate at ~3×10⁵/cm² on Matrigel in mTeSR1 + Y-27632 10 µM.

Day 0–2
Mesoderm
T (Brachyury) · MESP1
RPMI + B27 minus insulin + CHIR99021 6 µM (24 h pulse).
Day 3–5
Cardiac Mesoderm
ISL1 · NKX2.5 · GATA4
Switch to Wnt inhibition: IWP-2 5 µM or Wnt-C59 2 µM.
Day 7–10
Spontaneous Beating
cTnT · MYH6 · MYH7
RPMI + B27 (with insulin). Beating monolayer evident by Day 8–10.

RPMI + B27 minus insulin + CHIR99021 6 µM (24 h pulse). CHIR concentration is line-dependent (4–9 µM); titrate per line.

Day 10–14
Lactate Selection
cTnT · cTnI
Glucose-free RPMI + 4 mM lactate × 4–6 days. Eliminates non-CMs.

Glucose-free RPMI + 4 mM sodium lactate × 4–6 days. Non-CMs die because they cannot oxidize lactate. Validate >90% cTnT+ by flow.

Day 30–60+
Maturation
MYL2 · KCNJ2 · SERCA2a
Replate; mature with T3, IGF-1, fatty acids, electrical pacing or stiffness substrates.

Replate on PDMS or fibronectin in maturation medium with T3, IGF-1, fatty acids, dexamethasone. Apply electrical pacing (1–2 Hz) or stiffness substrate. Adult-like sarcomeres + KCNJ2/SERCA2a maturation.

  1. iPSC plating

    Single-cell dissociate; plate at ~3×10⁵ cells/cm² on Matrigel in mTeSR1 + 10 µM Y-27632.

  2. Wnt activation (Day 0)

    Switch to RPMI + B27 minus insulin with CHIR99021 6 µM for exactly 24 h. CHIR concentration is line-dependent (4–9 µM).

  3. Wnt inhibition (Day 3)

    Add IWP-2 5 µM or Wnt-C59 2 µM; refresh medium daily. Discontinue at Day 5.

  4. Cardiac induction (Day 7–10)

    Switch to RPMI + B27 (full); spontaneous contractions appear in 2–3 days.

  5. Lactate selection (Day 10–14)

    Switch to glucose-free RPMI + 4 mM sodium lactate for 4–6 days; non-CMs die. Verify >90% cTnT+ by flow.

  6. Maturation (Day 30–60)

    Replate on PDMS or fibronectin; mature in maturation medium (T3, IGF-1, dexamethasone, fatty acids); apply electrical pacing or stiffness cues.

>90%
cTnT+ after lactate selection
D8–10
spontaneous beating
60+ d
maturation window
96/384
screening-ready
02

Sarcomeres, Gap Junctions, Ion-Channel Maturity

I assess identity and maturation by IF for α-actinin/cTnT sarcomeric striations, MLC2v atrial-vs-ventricular subtype, and CX43 gap junctions. RT-qPCR panels track the MYH6→MYH7 fetal-to-adult shift; RNA-seq validates ion-channel maturity (KCNJ2, KCNH2, SCN5A, CACNA1C). For details see the dedicated Cardiomyocyte methods page.

cTnT cTnI α-actinin MYH7 MLC2v CX43 KCNJ2 SERCA2a
Flow Cytometry — % Marker-Positive after Lactate Selection
Mean ± SEM, n = 3 differentiations
Representative values from typical batches.
RT-qPCR — iPSC-CM Day 30 vs iPSC (log₂ FC)
ΔΔCt method · housekeeping: GAPDH, ACTB · n = 3
Bars above zero = up-regulated; bars below zero = down-regulated relative to undifferentiated iPSC.
03

MEA, Calcium & Optical Mapping

iPSC-CM monolayers are recorded on Axion Maestro multi-electrode arrays for beat rate, field-potential duration (FPD), and arrhythmia liability. Calcium transients (Fluo-4 or GCaMP6) capture systolic kinetics and dose-dependent QT prolongation by hERG blockers. Detailed assays appear on the cardiomyocytes page.

04

Impedance & Optical Contractility

Beating monolayers are profiled on impedance platforms (xCELLigence) for chronotropy and inotropy. Edge-detection algorithms quantify amplitude, frequency, relaxation time, and arrhythmia events at multi-well throughput. 3D engineered heart tissues (EHTs) and cardiac micro-tissues extend the assay to force generation under mechanical load.